INTRODUCTION:

The normal function of the heart is to provide the body with enough cardiac output so that the metabolic
needs of the peripheral issue should be meet. Heart failure is the failure of the heart to perform its normal
function. Heart failure is present when at normal or above normal filling pressures heart is unable to maintain
enough cardiac output to meet the metabolic needs of the peripheral tissues.
DEFINITION:
Heart failure is defined as:
The complex progressive clinic-pathological characterized by the failure
of the heart to generate enough cardiac output to meet the minimum
metabolic needs of the body tissues in-spite of normal or above normal
filling pressures.

EPIDEMIOLOGY:
In USA 5 million people have heart failure and every year about millions are added to them. Many of them
die as well. It is dominantly a disease of old age. Below the age of 60years about 1% of the population is having
heart failure but around the age of 80years about 10% of the population has heart failure. Population % in
elderly age is increasing so the disease burden related with heart failure is also progressively increasing.
PHYSIOLOGY:
CARDIAC OUTPUT:
It is the amount of blood ejected by ventricle during a unit time. In normal person the cardiac output is 5lit
approximately. Factors that determine the cardiac output are;
Strove volume
Heart rate
CO = SV x HR
HEART RATE:
It is define as the numbers of ventricular contraction per minute. (No. Of cycles/min)

STROVE VOLUME:
It is the volume of the blood ejected during one mechanical pumping or per beat. (Performance/ beat)
FACTORS THAT DETERMINE THE STROKE VOLUME:
Three most important determinant of strove volume are:
Intrinsic health of myocardium
Preload
After load



1) Intrinsic health of myocardium
All the diseases which affects the intrinsic health of myocardium up to an extent that will affect contractility of
myocardium and thus strove volume, will eventually lead to the failure of heart.
2) Preload:
It is the load or amount of blood which is present in the ventricular cavity at the end of diastole on which the
systolic power of the ventricle has to work and push the blood out. Initially if preload is increased slightly it will
increase the performance of the heart but if preload become too much than heart will fail to perform well and
there will be cardiac failure.
3) After load
It is the resistance against which the ventricle has to generate cardiac output. When resistance against heart
has to pump increases too much than heart will fail to work.
FRANKS STARLING LAW:
This law states that:
More you fill the ventricle, more it stretched out and more
strongly it will contract but with in physiological limits.
EXPLANATION:
Normally in healthy heart EDV is 140ml. if we keep on increasing the EDV it means heart is filling more. As
heart has intrinsic regulation thus more the EDV more stretches on myocardial fiber and there will be stronger
contraction and more it produces CO. it means in the healthy heart if we keep on increasing EDV, CO keep on
increasing.
PROBLEM WITH FAILING HEART ACCORDING TO FRANKS STARLING LAW:
If the heart suffers from MI than its power of contraction is decreased. It means for the given EDV the
generated CO is less.
LAPLACES LAW
This law states that:
Pressure generated by a cylindrical container is directly
proportional to the tension in the walls of container and
inversely proportional to the radius of container
EXPLANATION:
Pressure is required for CO. If there is no pressure generated in the lumen than there cannot be any cardiac
output. To build the pressure in the lumen there should be good tension in the walls. So tension in the walls
acting on radius eventually produces pressures.



PROBLEM WITH FAILING HEART ACCORDING TO LAPLACES LAW:
As heart is failing and neurohumoral mechanisms are retaining salt and water and increasing VR and EDV then
radius of the ventricle will increase. So with the given tension increasing radius will produces fewer pressures.
So neurohumoral mechanism in long run will dilate the heart to bigger radius due to which tension produced
will produces lesser pressures and less CO.
FACTORS WHICH FAILS THE HEART:
Following factors lead to the failure of the heart:
1) POOR HEALTH OF THE MYOCARDIUM
If the heart is not healthy but diseased than the diseased myocardium cannot perform well and it will lead to
failure of the heart.
2) INCREASED PRELOAD:
If we slightly increase the load on the heart it will cope with it but if we increase the preload too much than it
will lead to too much increase in radius of the ventricle that myocardium will not contract well and heart will
fail to perform.
3) INCREASED AFTER LOAD:
It the resistance against which heart has to work is increased too much than heart cannot generate enough
cardiac output and fails.
4) ABNORMAL NUMBER OF CYCLES:
The normal number of cycles heart performs per minute is 80. If number of cycles decreased too much than
required cardiac output cannot maintained and heart fails similarly if number of cycles increased too much
than due to very rapid pumping heart will not have enough time to take the required preload and start doing
empty cycle and heart fails.
5) ABNORMAL BODY DEMAND ON CARDIAC OUTPUT:
If body demand on oxygen and other nutrients increased too much that even increased cardiac output cannot
meet the body need than under these circumstances, heart will fail.
TYPES OF HEART FAILURE:
Heart failure is of following types:
1) High output heart failure
2) Low output heart failure
3) Left ventricular heart failure
4) Right ventricular heart failure
5) Bi-ventricular heart failure (congestive cardiac failure)
6) Systolic failure
7) diastolic failure


8) forward failure
9) backward failure
10) acute cardiac failure
11) chronic cardiac failure
12) cardiac cachexia

1) HIGH OUTPUT CARDIAC FAILURE:

It is the failure of the heart to fulfill the increased CO demands of peripheral body tissues. In this case the
heart is healthy but there is pathologically increase demand of body tissues on cardiac output and heart is
unable to meet the exacerbated demands of body tissues in-spite of doing increased work and producing
increased cardiac output. This is considered as high output cardiac failure. It is less common.

Causes:

a) THYROTOXICOSIS:
It is the condition in which peripheral metabolism is very high and demand of body tissue on oxygen and
nutrient supply is too much. Heart in-spite of doing extra work is unable to meet exacerbated demand of
our body and heart fails.

b) VERY SEVERE ANEMIA
Normal Hb/dl is 3gm/dl. In severe anemia hb/dl is very low and oxygen carrying capacity of blood is very
low. In order to provide the body tissue with enough oxygen heart has to step up the cardiac output.
Sometime inspite of increasing the cardiac output, increased oxygen demands is not fulfilled and heart
undergoes high output cardiac failure

c) PREGNANCY
In pregnancy, esp. when female has more than one baby in her uterus, women have to meet the demand
of her own body as well as she has to provide enough nutrients to fetus. So, demands of cardiac output
on her heart are more. If heart fails to meet the increased demand inspite of increasing cardiac output,
heart will fail.

d) PAGETS DISEASE
It is the disease of female genital organs, nipples and bones. In Pagets disease of bone, the catabolism
and anabolism of bones become pathologically rapid. The rapid metabolic turnover of bones requires lot
of blood flow and if heart fails to meet those increased demands it will lead to high output cardiac failure.

e) BERI BERI
Beri beri is due to deficiency of thiamine. In this disease, glucose breaks down partially and lot of lactic
acid is produced and many peripheral vessels dilate. Blood moves from atrial to venous site so rapidly
that enough nutrients and oxygen extraction cannot be maintained in capillaries. Some degree of arterio-
venous shunting occurs because of extremely low TPR. In such condition body requires more than normal
CO so that during every extra cycle some nutrients should be provided.






f) AV- FISTULA
Arterio-venous fistula is made for dialysis. In AV-fistula blood directly shut to venous site and this blood
do not play role in delivering oxygen. So to meet the requirement of peripheral tissue there should be
increased cardiac output because some of the cardiac output has been wasted due to AV shunting
without delivering oxygen and nutrient to microcirculation.

2) LOW OUTPUT CARDIAC FAILURE:

It is the condition in which peripheral demand on cardiac output is normal but heart is unable to maintain
even the normal cardiac output.
Causes:

Contractility failure
Preload problem
After load problem
Rhythm problem

a) MYOCARDIUM CONTRACTILITY FAILURE:
It may be due to intrinsic problem or extrinsic problem

Intrinsic problem:
It is the problem with the myocardium either the function of the myocardium is loss or the mass of the
myocardium is loss i.e.; myocardium is not healthy and thus not contracting well.
Intrinsic problem includes

IHD:
It is the most important cause of reduced function of myocardium. If large or multiple areas in myocardium has
undergone infarction and replaced by fibrotic tissues it means myocytes are lost. Such ventricle has not normal
contractility power due to this heart will not generate even normal CO and this will lead to LOCF.


Hypertrophic or dilated heart:
Due to hypertrophy and dilation heart cannot pump well and CO is less than normal and this again leads to
LOCF.

Infiltrative disease:
In this disease an abnormal protein (amyloid) is deposited in the myocardium and due to which the
normal contracting power of myocardium is lost eventually required CO cannot be generated by
heart.

Hemochromatosis:
In this disease extra hemosiderin is deposited in myocardium and produces toxicity to myocardium
and myocardium do not contract well eventually patient go into LOCF.

Extrinsic problem:
It is the problem in which the myocardium is itself healthy but some external factors have suppressed
its performance and this myocardium is unable to contract well.
External contractility suppressing factors are:
Drug (cardio toxic drugs)
Some drugs as extrinsic factor may produce damage to myocardium and thus reduces its contractility
and LOCF occur.
e.g.:
doxorubicin
toxicity of -ve ionotropic drugs (antiarrhythmic)

metabolic acidosis
Severe metabolic acidosis reduces the myocardial contractility
Alcohol:
The high concentration of alcohol leads to cardio toxicity and suppresses the myocardium
contractility and leads to LOCF while low concentration is beneficial for coronary artery disease.
a) Preload problem:
If preload increases, than initially CO also increases, but if preload is too much than CO decreases.
Because when preload is more, heart is under volume-work overload (volume against which LV has to
work is excessive) and if this increased volume stretches the myocardium beyond physiological limits


and increases the radius of ventricle dangerously than inspite of good tension this dilated ventricle is
unable to generate enough pressure to push the blood in the atrial tree. So, heart goes into LOCF.
Causes of excessive preload:
1) Valvular diseases:

a) Mitral/tricuspid regurgitation:
In the patient having mitral or tricuspid regurgitation, when ventricle contracts not only it pushes
the blood to normal pathway but also leads to regurgitation and waste some of its efforts and
some blood leaks into atrium. In such cases during systole atrium is filled by lungs as well as from
ventricle so atrium during systole is overloaded. Now during diastole when ventricle relaxed, high
amount of blood comes in the ventricle. It is occurs chronically than ventricle will undergo volume
overloads and this will leads to hypertrophy and dilatation both. Dilated ventricle has more radius
and thus at the given tension it produces less pressures. So this ventricle is less efficient and low
output generates and this will lead to LOCF.
b) Aortic/pulmonary valve regurgitation:
Normally when ventricle contracts tricuspid valve closes and aortic and pulmonary and blood
ejects and when ventricle relaxes pulmonary and aortic valve closes and mitral and tricuspid valve
open. If a patient is having pulmonary or aortic valve regurgitation than these valve do not closes
during systole and some of the ejected blood falls back. So, now during diastole blood not only
moves from atrium to ventricle but also from aorta to ventricle and this leads to volume overload
and ventricle become dilated poor pump and decreased CO is generated and this leads to LOCF.
c) After load problem:
When after load is more than heart has to work against high resistance and pressure load is more
and ventricle will undergo hypertrophy. Hypertrophic myocardium is thick but when ventricle
cannot generate enough pressures to meet the outflow resistance then they start dilating and
heart will than fail.
Causes:
1) Systemic HTN is most important cause of LV failure and pulmonary HTN is most important
cause of RV failure. Due to HTN ventricle has increased after load and when heart cannot
generate enough pressure to meet with after load than it will undergo failure.
2) Aortic stenosis
3) Hypertrophic obstructive cardiomyopathy
4) Coarctation of aorta

d) Rate and rhythm problem:
a) Severe Brady arrhythmias:
In this heart rate is so slow that heart cannot maintain required CO and leads to LOF.
b) Severe tachyarrhythmia:
In this heart rate is so fast that total cardiac cycle time is dangerously reduced esp. diastolic time is
so much reduced that ventricle do not relax for enough time to fill properly. If they do not fill
properly they cannot pump properly and CO reduced and LOF occurs. It involves RVF & LVF
simultaneously.
3) LEFT VENTRICULAR CARDIAC FAILURE:
Left ventricular failure means that LV is unable to maintain enough CO to meet the demand of body
in presence of normal or above normal filling pressures.
CAUSES:
Myocardial dysfunction (e.g.: MI)
Excessive preload (e.g.: MR and AR)
Excessive after load (e.g.: S-HTN & P-HTN)
Rhythm problem
First three leads to isolated LVF not involving RH but rhythm problem leads to both RVF and LVF
simultaneously.
MECHANISM:
When LV is not working well than whatever EDV is in ventricle, ventricle is unable to eject enough
fraction of it. So ejection fraction reduces from normal 0.5 to <0.35. When ventricle receive more and
pump less so it will dilate. When EDV is pathologically more than ED pressures are also more and atria
cannot easily empty into ventricle because ventricle is already overfilled. Due to this overfilling when
during diastole overfilled ventricle receives extra amount of blood an added sound come called S
3
. So
S
3
is the earliest feature which shows that heart is undergoing volume overload. If at the top S4
appears it means atria is doing excessive effort to push the blood in ventricle. Addition of S3 and S4 in
LV shows the onset of LVF. S3 and S4 shows volume overload and pressure overload respectively.
COMPLICATIONS OF LVF:
When atria instead of high pressure cannot push the blood in ventricle than back pressures will go to
pulmonary circulation and pulmonary vein volume and pressure both go up and this will lead to
pulmonary edema. Following are the complications of LVF.


Interstitial edema:
RH is pumping blood into pulmonary arterial tree and arterial tree is feeding into capillary system but
capillary system is unable to drain into venous system and to LV so back pressures go up to
pulmonary microcirculation. When hydrostatic pressure in the pulmonary capillaries become very
high than fluid will start oozing out of pulmonary capillaries and when excessive fluid oozes out, it will
lead to interstitial edema initially because fluid will appear only in interstitium initially.
Alveolar edema:
When edema become so much that even excessive fluid appears not only in interstitial area but also
in alveoli, it will lead to alveolar edema. Pressures are high in pulmonary arteries, pulmonary veins
and pulmonary capillaries but only pulmonary capillaries will leak because they are thin walled.
Pulmonary circulation is congested or edematous and lungs become heavy and boggy.
Bronchial edema:
In this, bronchial mucosa becomes edematous and it produces irritation to bronchi. This irritation
may lead to dry cough.
CLINICAL FEATURES OF LVF:
LVF leading to back pressure in lungs and it leads to pulmonary congestion and edema. Due to
chronic irritation to peri-capillary areas fibrosis may start an even there may be reflect arteriole-
constriction of pulmonary tree and RH find it difficult to push blood into high resistance system so
pulmonary HTN start and RV undergo hypertrophy, dilation and fails. If RV yet not undergone
hypertrophy and problem is limited only to LV and feature are related with pulmonary congestion
and edema which are as follows:
Dyspnea
It is the problem when there is difficulty in breathing which is unpleasant. It is mainly due to
heavy and boggy lungs when musculoskeletal system has to over work to maintain inspiration and
expiration all the time.
Orthopena:
If the patient is sitting than gravity will pull the fluid in lower art of the lungs and upper part of the
lungs are relatively dry so breathing function is well done in upper part of the lungs. But when this
patient lies down than edema fluid is evenly distributed in whole lungs so this problem of dyspnea
becomes more. Thats why such patient likes sitting posture. When dyspnea becomes worse on
lying down, it is called orthopnea. It is more sever stage of pulmonary edema.
paroxysmal nocturnal dyspnea (PND)
When these patients are sleeping, they suddenly wake up with sever restlessness and gasping
from air, it is called PND. When these patients lay down, venous return to R-heart increases and
RH keep on increasing CO to lungs and as lugs cannot pump blood to LH so edema become more
worse.



Chronic cough:
It occurs due to bronchial edema and when capillaries in bronchial system rupture frothy pink
sputum is produced.
Cardiac wheezing:
Sometimes in LVF bronchial edema becomes so severe that air flow become obstructive like
situation develops. It occurs due to swelling of bronchi when lumen of bronchi becomes narrow.
These narrow lumen act as whistle so when air passes thru that lumen esp. during expiration they
act as powerful whistle because during expiration usually bronchi become narrow and due to
edema it become further narrow. So, musical whistling sound comes from the chest. It is due to
cardiac dysfunction, so we call it cardiac wheezing.
End inspiratory crepitation:
When we ascultate the base of lungs and lungs are having alveolar edema than end inspiratory
fine cracking sounds (fine crept) will come because wet alveoli open and close with sound.
4) RIGHT VENTRICULAR CARDIAC FAILURE:
Isolated RVF is very rate and less common. Most if the cases of RVF are secondary to LVF. When
LVF is for longer duration it will lead to pulmonary HTM and that may result into RVF. RVF is not
working well there is back pressure in systemic circulation and portal circulation.
Causes:
1- LVF
2- Pulmonary HTN (which is due to some primary diseases of lungs like fibrosis of lungs) in such
cases, it become difficult for RH to pump blood into lungs under pressure overload and it will
undergo hypertrophy and eventually dilated and fails. Such condition is called cor- pulmonale)
Cor-pulmonale:
RV hypertrophy dilation and eventually failure due to pulmonary HTM but this pulmonary HTN
is due to LVF. All the conditions which lead to pulmonary HTN excluding LVF leading to RVF
are called cor-pulmonale.
3- Pulmonary stenosis which is leading to pressure overload in RH and pulmonary valvular
regurgitation which is leading to volume overload in RH.
4- Diseases which is intrinsically providing problem with RV muscles.
5- Tricuspid regurgitation which is leading to volume over load.


Complications:
When there is RVF due to any causes, following complications occur.
a- INCREASES JVP:
Whenever there is RVF initially pressure in RV goes up and it become difficult for RA to empty into
RV do pressure in RA goes up that result in inability of cable system to drain well into RA so JVP
goes up but pulse pattern shows elevation in a-wave because of strong contraction of atrium
against hypertrophic ventricle.
b- Hematomegaly:
When RVF occurs, pressure in cable system goes up. One of the manifestations of IVC pressure
going up is that there is impairment of drainage of hepatic veins into IVC. It is leading to edema of
liver. So there is hepatomegaly with R upper quadrant pain sometime.
c- Pulsatile liver:
If RVF is due to tricuspid valve regurgitation than RV will contract and give a very strong wave in
SCV and IVC. JVP become every elevated that c and v wave accumulate. When there is strong
back pressure in IVC it leads to strong pressure in liver and with every RV contraction live will
move. It is pulsatile live along with enlargement. Every pulsatile live is not due to tricuspid
regurgitation.
d- Splenomegaly:
When liver cannot drain into IVC than pressure in liver is so high that portal system cannot drain
into liver so portal HTN develop that may lead to slenomegaly b/c spleen cannot drain well.
e- GIT edema:
Blood is brought to GIT from systemic arterial tree but it cannot drain from GIT so GIT become
edematous which leads to mal-absorption, anorexia, nausea, taste loss etc.

f- Acities:
When portal blood is coming to liver but from liver blood cannot drain so pressure in sinoside
become more. Due to increases pressure more fluid oozes into interstitium and more lymph is
form. This lymph may oozes out of liver and may add to the fluid in the peritoneal cavity. It is
called asicites (excessive oozing of blood from liver capsule and from GIT serosa)
g- Generalized edema:
Normally blood is pumped into systemic capillaries by LV and these capillaries drain into venous
cable system. When RV failure occurs there is high pressure in RV, RA and cable system and blood
from systemic capillaries cannot drain well into cable system b/c of high back pressure in veins of
body. All the systemic circulation becomes congested (overloaded with blood). First systemic

capillaries become congested than hydrostatic pressure become so high that fluid start oozes
form everywhere capillaries. This edema is present all over the body except lungs, we call it
anasarca or extreme generalized edema. This is dependent edema and pitting edema (leave a
dent on skin when you press the area with finger). Gravity redistributes edema in body. In day
time while walking edema is in lower part o the body and when laying down on bed edema is in
back (in supine position).
5) BI- VENTRICULAR CARDIAC FAILURE: (CONGESTIVE CARDIAC
FAILURE)

When in patient both ventricle are failing it means pulmonary system is congested as well as
system is also congested. All the circulation in the body is congested o well call it congestive
cardiac failure or biventricular failure.
6) DIASTOLIC CARDIAC FAILURE:

Basically healthy ventricle should have two functions:
1) During diastole ventricle should relax enough to receive the blood.
2) Once received enough blood it should contract enough to maintain proper CO
In some cases ventricle do not relax properly and is not complaint as they should be and ability of
ventricle to undergo proper relaxation and accommodation of enough EDV (diastolic function) is lost.
It is called Diastolic failure. In diastolic failure EDV is low and EDP is high.
Causes:
a- LV or RV hypertrophy:
When ventricle is chronically working against pressure overload like aortic and pulmonary
stenosis, HTN than naturally LV or RV undergoes pathological hypertrophy alone. During
pathological hypertrophy newly added muscle mass is formed in the interior of ventricle and
lumen of ventricle reduced. When ventricle is thick it does not relaxes properly. It means its
ability to receive enough EDV is reduced and they cannot maintain good CO. when ventricle
undergo this type of problem we say there diastolic failure. If chronic pressure remain elevated
than, hypertrophic ventricle dilate.
b- Amylodosis:
It is rare condition in which lot of amyloid proteins are deposited with in myocardial tissue.
Myocardial tissue become stiffen and then during diastole it cannot relaxes and cannot
accommodate enough amount of blood and heart undergo diastolic failure.
c- Early phase of HOCM:


In such cases there is asymptomatic hypertrophy of LV i.e) hypertrophy on septum side. In that
case also it become difficult to fill the ventricle and patient may undergo initially diastolic failure.
Clinical feature:
One of the most important clinical features is that there may be S
4
because atrias are contracting
against unyielding stiffened ventricle/ hypertrophic ventricle. (S
1
+S2+O+S
4
) (S
4
gallop)
7) SYSTOLIC CARDIAC FAILURE:
Systolic failure is present when ventricle contractions are week. Every time in diastole whatever
blood ventricle receives, it is unable to pump properly and keep on accumulating fluid that will lead
to high EDV and high EDP.
Causes:
a- IHD:
It mostly causes systolic failure and less often produces diastolic failure.
b- HTN:
Initially it causes diastolic failure but if diastolic failure and HTN is not controlled than heart undergo
dilatation and eventually systolic failure.
c- Use of ve ionotrpic drugs:
Negative ionotropic drugs include antiarrhythmics, beta blockers and Ca channel blockers. Due to
these drugs heart will relax well but contract poorly and leads to systolic failure. Patients, who are
under extensive therapy of ve ionotropic drugs, toxicity of these drugs, will lead to systolic failure.
Clinical feature:
In SF there is rapid ventricular filling during diastole in overfilled ventricle and that may produce a
sound called S
3.
(S
1
+S
2
+S
3
+O) (S
3
gallop).
In advance stages of CF there may be (S
1
+S
2
+S
3
+S
4
) (full gallop) and sinus tachycardia.
Diastolic failure has better prognosis but systolic failure is more common.
8) BACKWARD FAILURE:
This term is very commonly used when we are using symptomatology of cardiac failure. Backward
function of LV is to prevent the blood from going backward to lungs and of RV is to prevent the blood
from going back to systemic tree. When LV and RV fails to perform its backward function it is called
backward failure.
LVF leading to backward failure:


When LV fails to perform its function than EDP are always high due to that reason back pressure is
there in atria and that back pressure lead to the trouble in pulmonary circulation and pulmonary
edema and congestion occurs and related clinical feature develop. These all happen due to backward
flow of blood.
The blood proximal to failure point moves backward and pulmonary circulation become congested
and edema occur.
RVF leading to backward failure:
When RV is failing blood will accumulate in RV and EDV become very high and eventually pressure
will become very high atrium cannot drain well so there will be back pressure and all the veins in
systemic tree become congested and related clinical features develop. All these are due to backward
failure of RV.
9) FORWARD FAILURE:
Forward function of LV is to allow the blood to move toward aorta and of RV is to allow the blood to
move toward lungs. When LV and RV fails to perform its forward function it is called forward failure.
LVF leading to forward failure:
When CO become very poor in forward arterial system than body tissue are under perfused and due
to that certain clinical feature develops like fatigability. These features of fatigability are due to
forward component of LV failure.
RVF leading to forward failure:
When RV is failing and less blood is moving to pulmonary circulation and there is poor oxygenation of
blood than there is forward failure of RV.
10) ACUTE CARDIAC FAILURE:
Acute cardiac failure means sudden failure of the heart.
Clinical features:
There are two presentation of acute CF.
1- Acute pulmonary edema of cardiac origin.
Some patient undergoes sudden CF if dominant clinical feature are related with pulmonary
edema. It means real problem is dyspena, orthopnea, PND.
2- Cardiogenic shock
Some patient undergo sever cardiac damage and sudden cardiac function loss like BP is rapidly
going down and patient develop feature of shock. This type of acute failure is called cardiogenic
shock.

Causes:
1) Massive MI:
In some patient there is large area of MI present in myocardium. This type of problem occurs when
someone has coronary artery disease and sudden a big thrombosis form and there is total occlusion
of coronary system than a large area of myocardium undergo infarction. This infracted area does not
contract at all or contract very poorly and there form a hard area of hypokinesis (decreased
movement) or dyskinesia (abnormal movement) than CO dramatically drops and it leads to acute
cardiac failure.
2) Sudden failure of valve:

a- Valvular regurgitation:
If that part of myocardium to which papillary muscle are anchored undergone infarction then
overlying papillary muscles either itself undergo infarction or become dysfunctional or even it
may undergo rupture. If papillary muscles detach from its attachment then during systole mitral
valve start regurgitation and lead to acute cardiac failure.
b- Aortic valve failure:
In infective endocardititis vegetation loaded with lot of bacteria is formed on the aortic valve.
These bacteria produce destructive enzymes and at the same time, due to inflammatory process,
lot of neutrophils also releases destructive enzymes. These all destructive enzymes leads to
destruction of leaflet of valve an than during diastole this valve cannot prevent back flow so form
aortic valve there is sever aortic regurgitation and that may lead to acute cardiac failure.
3) Ventricular septal defect:
If MI involve the septal area and this septal area undergo rupture then there is sudden development
of VSD and it leads to acute CF due to sudden loss in cardiac function
4) Acute pulmonary thrombo-embolism:
This problem is seen in deep venous thrombosis. In this condition form a lower limb a large
embolus move along the venous blood toward the RH and may pass through atrium to ventricle
and eventually into bifurcation of pulmonary artery. If this large thrombus gets stuck in
pulmonary artery than large part of pulmonary circulation is block and RH will undergo sudden
failure b/c it cannot push the blood against such high resistance. This situation lead to acute CF.
Here LV is not failing, the real failure is in RV b/c LV failure is when blood filling is normal or above
normal but still CO is not maintain and here LV is not receiving enough blood to pump.
5) Cardiac temponade:
It is a condition in which there is so much fluid accumulation in pericardial cavity that there is
circulatory collapse. After infarction when a part of myocardium undergo destruction and rupture
than massive amount of blood will accumulate into pericardial sac with every beat but
pericardium cannot distant too much due to rapid accumulation of blood so pericardium will
compress both ventricles and JVP goes up as venous blood cannot drain into RH and as LV cannot
push well so systemic BP reduces and on auscultation heart sound are distinct and muffeled. This
type of situation is called cardiac temponade and this lead top acute cardiac failure. It is
something like CCF.
11) CHRONIC CARDIAC FAILURE:
Chronic cardiac failure means failure of the heart after long process.
Causes:
IHD
HTN
Alcohol related myocardial condition
These conditions involve the heart for long time and eventually patient develop progressive
syndrome of chronic heart failure.
12) CARDIAC CACHEXIA:
It is severe cardiac failure and usually lasts more than 5 years. Some of these patients develop
very severe generalized wasting of body esp. loss of lean mass of the body (loss of non
edematous tissue). If patient if having CCF and using diuretics so lot of fluid is lost and patient
weight is reduced, it is not cachexia.
Causes:
a) Patient who have sever CHF for long time than in these patients there will be:
Anorexia, that leads to less input of nutrients.
Mal-absorption, in which whatever the nutrient is taking by patient is not digesting
and absorbing.
Excessive loss of nutrient form GIT and from renal system
Patient anabolic rate is low (formation of new proteins in body is significantly reduced)
Metabolic rate is very high (increasing metabolism requires more nutrient and nutrient
are less available)
All these leads to significant loss of lean body mass and patient become bony. If edema is present, it
will keep the pt swollen otherwise lean body mass is very less.
b) In these patients there is an increased circulating level of tumor nacrotic factor. TNF has
receptors on hypothalamus and by acting on hypothalamnus if alters the metabolism in
patients it decreases anabolism than increases the catabolism, it leads to weight loss.


Reasons for the presence of excessive TNF in blood:
1) B/c of poor peripheral circulation in which there is generalized hypoxic or hypo perfusion
condition into tissue which lead to formation of excessive TNF.
2) Failing myocardium itself may produce excessive amount of TNF.
PATHOPHYSIOLOGY OF CCF:
1) Initial insult to cardiac function
2) Onset and triggering of compensatory mechanism
3) Advantages of compensatory mechanism
4) Disadvantages of compensatory mechanism
5) Progressive irreversible CCD syndrome.

1) Initial insult to cardiac function:
If the initial insult is massive MI and if patient survive the initial insult and remain untreated than
within few weeks, infracted area I replaced by fibrotic band (scar) b/c of hypokinesia (decreased
movement) and dyskinesia (abnormal movement) and eventually its power of contractility is
reduced and LVF is started in this patient.
Once LVF starts, there are elements of backward failure and forward failure. Forward failure leads
to fatigue and less tolerance of exercise while backward failure leads to pulmonary congestion
and edema. If it remains for long time it will lead to pulmonary HTN which leads o hypertrophy
and dysfunction of RV. RV dysfunction leads to increased JVP, hepatomegaly, ascities and
generalized edema. In such cases when initial insult leads to CCF.
2) Onset and triggering of compensatory mechanism
Following compensatory mechanisms are activated to help the biological system once CF started:
a- Sympathetic adrenergic stimulation
b- RAAS stimulation
c- ADH release
d- Endothelin release
e- Excessive release of ANP and BNP
f- LVH

a- Sympathetic adrenergic stimulation
When CCF starts, this will leads to decrease CO and decreased perfusion to many organs including
carotid sinus and carotid sinus pressure goes down. When BP drops in carotid sinus system this
will stimulate CNS and there will sympathetic outflow and increased sympathetic outflow leads
to:

i) Stimulation of SA node and this leads to increased HR. when there is increased HR it
means sinus tachycardia is present and this will increase CO and try to compensate partly
for the reduction of CO.
ii) Stimulation of myocardium of LV and RV. It is +ve ionotropic stimulus and it leads to
increase contractility and increased SV and increased CO.
iii) Stimulation of adrenal medulla and it leads to release of lot of epinephrine in circulation.
Adrenaline act on adrenergic receptors and its will increased HR and increased SV.
iv) Stimulation of smooth muscles in veins and there will be significant vasoconstriction. Veins
are capacitance vessel (they contain lot of blood in them). When veins constrict VR to
heart is increased, length if myocardial fiber will increased and heart contract strongly so
SV increased.
v) Stimulation of smooth muscle of arteries and arterioconstriction occur. Arterioconstriction
redistribute blood to most vital organs so that vital organs get perfused on preferential
rate. Arterioconstriction to splenic circulation, renal circulation and cutaneous circulation
under sympathetic stimulation occur but there is no coronary and cerebral circulation
involvement.

b- Renin angiotension aldosterone system:
When CCF start, CO decreases and sympathetic NS leads to constriction of renal vessels than
there will be significant drop in renal perfusion. Kidneys will response to this hypo perfusion by 2
mechanisms:
By increase release of rennin
By reducing GFR

By increase release of rennin
By decreasing perfusion to kidney, RAAA stimulates and more rennin is released by JGA in general
circulation. Rennin will act on angiotensiogin (ATG) and convert ATG to angiotensin I (AT-I). AT-I
when passes through liver it acted upon by ACE and converted into AT-II. AT-II has following
functions:
It stimulated sympathetic NS which in turn leads to increased HR and increased contractility.
It stimulates veins. Veins have AT-II receptors and when these receptors are stimulated, it will
lead to venoconstriction which lead to increased VR to heart and increased CO.
It stimulates arteries. Arteries also have AT-II receptors and when these receptors are
stimulated, it will lead to arterioconstriction which leads to redistribution of blood to more
vital organs like myocardium, cerebral vessels because these vessels are not under significant
sympathetic constriction effect.
When AT-II works on adrenal medulla, it stimulates the release of aldosterne form zona
glomerulosa. This aldosterone will act on principle cells on distil convulated tubule and help to
retain more salt and water and aldosterone mediated salt and water retention occurs.


By decreasing GFR:
When GFR is reduced, due to decreased perfusion of kidney than less filtrate will pass slowly from
proximal convulated tubule and PCT has more chance to retain salt and water. Initially this salt
and water is good and blood volume increases.
c- ADH release
ADH is antidiuretic hormone. The release of ADH leads to:
i) Retention of water and salt by working on last part of nephron. Last part nephron is more
porous to water and more water is pulled back to renal interstitium and leads to water
retention and blood volume increased.
ii) In increased concentration ADH is also called vasopressim. It leads to vasoconstriction.
Venoconstriction increased venous return and increased CO while arterioloconstriction
increased perfusion of blood to most vital organs.

d- Endothelin release:
When there is CCF then pulmonary endothelial cells releases endothelin. It is strong
vasoconstrictor and leads to generalized vasoconstriction and it also lead increased sympathetic
outflow. It also leads to stimulation of RAAS and also leads to LVH. They are also beneficial initially
but not in long run.
e- Excessive release of ANP and BNP:
BNP is ventricular NP. It was initially discovered in brain. In CCF atria and ventricle both release
excessive amount of ANP and BNP respectively.
They try to counter the dangerous effect of other compensatory mechanism,
e.g:
If salt is more retained in body than BNP and ANP produces natriuresis.
If water is more retain in body than BNP and ANP produces diuresis.
If vasoconstriction is too much than BNP and ANP produces vasodilation
If RAAA is too much stimulates BNP and ANP inhibit that.

f- LVH(
LVH is compensating mechanism but in initial stage of CF.
3) Advantages of compensating mechanism:
Compensating mechanisms are triggered by low CO and has following advantages:
All compensating mechanisms together are producing direct stimulation of SA node, +ve
ionotropic effect and increased CO.

They produce venoconstriction and increased venous return to heart and increased EDV
and increased CO.

They produces selective arterioconstriction and redistribute blood to more vital organs,

They also lead to salt and water retention which increase BV, VR and CO.

These all the beneficial in early stages but in long run they are harmful.

4) Dis-advantages of compensating mechanism:
If we dont control the compensatory mechanism pharmacologically, then they develop certain
disadvantages. Following are the disadvantages of neurohumoral activation.
Chronic excessive preload:
Due to compensatory mechanism when there is chronically increased BV and increased
venomotor tone than there is chronically over filing of ventricles. It means ventricle is chronically
exposed to excessive preload.
Chronic excessive after load:
Due to compensatory mechanism when there is chronically increased vasomotor tone and vessel
remain constriction (arterioloconstriction). It means ventricle is chronically exposed to excessive
after load.
Both of these will lead to remodeling of ventricular tissue.
5) Progressive irreversible CCF syndrome:
Remodeling involves:
Excessive loss of myocardium (apoptosis)
When there is adrenergic stimulation it is over stimulate the myocardium and eventually
myocardium undergo apoptosis
Fibrosis:
Extracellular matrix produces more protein and fibrotic tissue.
LVH:
Some myocardial cells are destroyed and remaining undergo hypertrophy
Functional problem involves:
Due to chronic activation of neuro-humoral factor it will increase preload and after load for long
time and this will start damaging myocardium and there is some degree of hypertrophy which is
pathological hypertrophy. This will lead to abnormal expression of genes. Due to chronic stress to
myocardium there is altered genomic expression means myocardium expresses their genes in
altered fashion and start producing different types of abnormal or unusual proteins. Genes start
expressing:
Proteins which are usually expressing during fetal life or early life and are not usually
expressing during fetal life or early life and are not so good functional.
Abnormal proteins as well
This genomic expression/ alteration in myocardial cells even though lead to larger, elongated
myocardial but not healthy myocardial cells. These myocardial cells are loaded which abnormal
proteins.
e.g.:
Ca handling proteins become abnormal.
Normally during systole Ca is released from sacroplasmic reticulum into cytosol than ventricular
cells contract while during diastole there is re-uptake of Ca from cytosol back to sacroplasmic
reticulum. These Ca handling protein which handle the release and reuptake of Ca are distributes
and become abnormal in hypertrophic heart or heart with CCF.
MANAGEMENT: