physio 17 cardiac pathophysiology 2

7/27/2019 Physio 17 Cardiac Pathophysiology 2

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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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Infarction 2 / 5

Immediate response

Baroreceptor response

Chemoreceptor Response

CNS ischemic response


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Infarction 3 / 5

Sympathetic stimulation

Strengthens the heart

Raises the Psf


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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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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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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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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



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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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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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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



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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,

physio 17 cardiac pathophysiology 2

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