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Cardiac Failure

Cardiac Failure
The failure of the heart to pump enough blood to satisfy the 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 blood flow. Other causes are Damaged heart valves -External pressure around the heart. -Vitamin B deficiency. -Primary cardiac muscle disease -other conditions that makes the heart a hypoeffective 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

Progressive Changes After Myocardial Infarction 3 / 5

Sympathetic stimulation Strengthens the heart Raises the Psf

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-thirds normal. Low cardiac output + Low arterial pressure = low urine output. Moderate increase in body fluid and blood volume is an important factor in helping to compensate for the diminished pumping ability of the heart by increasing the venous return. The increased blood volume increases venous return in two ways (1) it increases the mean systemic filling pressure, which increases the pressure gradient for causing venous flow of blood towards the heart, (2) it distends the veins which reduces the venous resistance and allows even more ease of flow of blood to the heart. Detrimental effects of excess fluid retention in severe cardiac failure, which include 1)Overstretching the heart ,thus weakening the heart still more. 2)Filtration of fluid into the lungs causing pulmonary oedema and consequent deoxygenation of the blood. 3)Development of excessive oedema in most parts of the body.

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 more and more edema and.. finally death.
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Decompensated Heart Disease With Increase In Right Atrial Pressure

As more & more fluid is retained, the Psf goes on rising, & the Right Atrial pressure goes on rising.
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Decompensated Heart Disease With Increase In Right Atrial Pressure

Soon, the rising edema causes edema of the heart muscle & stretching of the myocardium further deterioration of cardiac functionclinically this is seen as Pulmonary edema 11

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 excrete daily the necessary amounts of fluids.

Vicious Cycle Of Cardiac Deterioration


The low Arterial pressure consequent to Cardiac Shock results in reduced coronary supply. This is confounded with the already existing Coronary 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 of Hypotension.

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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 Digitalis strengthens the heart, so that the heart becomes strong enough to pump adequate quantities 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 renal tubules. 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 decreases urine 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 most powerful stimuli known for aldosterone secretion and potassium concentration rises in response to reduced renal function in cardiac failure. Atrial natriuretic factor is a hormone released by the atrial walls of the heart when they become stretched. The ANF then has direct effect on the kidneys to increase greatly their excretion of salt and water, therefore playing a natural role to help prevent extreme congestive symptoms during cardiac failure.

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, physical damage 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

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Mechanism Of Action Of Digitalis

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High Cardiac Output Failure


AV Fistula & Beriberi

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High Cardiac Output Failure


AV Fistula & Beriberi

In AV fistula-there is overloading of the heart because of excessive venous return , even though the pumping capability of the heart is not depressed. In Beriberi heart disease( lack of thiamine)the venous return is greatly increased because of diminished systemic vascular resistance but at the same time, the pumping capability of the heart is depressed.

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 heart defects

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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 heart sounds. 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 & 2nd Heart sounds were believed to be produced 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 3rd Heart Sound is: Produced at the beginning of middle 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

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Valvular Lesions
The left heart valves have higher incidence of valvular lesions than the right heart valves because of 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
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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 A haemolytic streptococci. Large haemorrhagic ,fibrinous, bulbous lesions grow along the inflamed edges of the heart valves. The mitral valve most often seriously damaged, followed by aortic valve.( high pressure stresses responsible for frequency on the left heart )

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Aortic valvular disease


In aortic stenosis, the contracting left ventricle fails to empty adequately, whereas in aortic regurgitation, blood flows 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 output of 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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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 left ventricle 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


Aortic stenosis
a nozzle effect is created during systole, with blood jetting at tremendous velocity through the small opening of the valve leading to a loud, harsh, ejection systolic murmur and thrill (palpable murmur) due to the turbulence.

Aortic regurgitation
during diastole, blood flows backward from the highpressure aorta into the left ventricle, causing a "blowing" murmur of relatively high pitch with a swishing quality heard maximally over the left ventricle (diastolic murmur) Very much increased pulse pressure
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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, much of 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 the left 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


The high left atrial pressure in mitral valvular disease also causes progressive enlargement of the left atrium, which increases 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 almost double the normal pressures This, in turn, causes hypertrophy of the right side of the heart, which partially compensates for its increased 45 workload.

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 low rumbling 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 46 (pan/holo systolic murmur)

Congenital Anomalies
They are usually categorized under the following headings: 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 backward from 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 circulation called a leftto-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 called right-to left shunt.
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Fetal Circulation

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Fetal Circulation
Lungs are collapsed and the elastic compression of the lungs 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 the pulmonary 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 allows immediate 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
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 is twice 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.
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Fetal Circulation

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Patent Ductus Arteriosus

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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.
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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, 57 but less flow through the stenosed pulmonary artery.