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Heart failure is an abnormal clinical
syndrome that involves inadequate pumping
& feeling of heart.
(Lewis’s)
In heart failure heart is unable to provide
sufficient blood to met the oxygen need of
the tissue
Worldwide 2 crore people are affected by
heart failure.
Approximately 2% prevalence in developed
countries.
Women are more survival then man
Coronary artery disease is the major cause
for HF.
The major cause of HF may be divided into two
sub groups, those are:-
I. Primary cause
II. Precipitating cause
Coronary artery disease
Hypertension
Rheumatoid heart disease
Congenital heart defect(Ventricular septal
defect)
Pulmonary hypertension
Cardiomyopathy( Viral, substance abuse)
Anemia
Infection
Thyrotoxicosis
Hypothyroidism
Dysrhythmias
Bacterial endocardiatis
Pulmonary emboilism
Pagets disease
Neutritional deficiency
Hypovolemia.
Anemia:- In anemia there is decrease o2 carrying
capacity of blood which stimulate increase in cardiac
output to meet the tissue demand. This leads to
increase in cardiac workload & increase in size of LV.
Infection:- In infection there is increase in O2 demand
of tissue stimulating increase in CO.
Thyrotoxicosis:- Change in the tissue metabolic
rate,increase HR & workload of the heart.
Hypothyroidism:- Indirectly pridispose to
Atherosclerosis, severe hypothyroidism decrease
myocardial contractility.
Dysrhythmia:- May decrease CO and increase wark
load & O2 requirment of myocardial tissue.
Bacterial Endocardiatis:- It cause increase metabolic
demand & O2 requirmentof myocardial tissue. It also
cause valve dysfunction which causes stenosis &
regurgitation.
Pulmonary Emboilism:- Increase pulmonary pressure
resulting from obstruction leads to pulmonary
hypertension, decrease CO.
Pagets Disease:- Increase workload of heart by increase
vascular bed in the skeletal muscle.
Nutritional Deficiency:- May decrease cardiac function
by decrease myocardial muscle mass & myocardial
contractility.
Hypovolemia:- Increase preload causing volume
overload on the right ventricle.
II. Right side failure vs left side failure
Left side failure:-
It results from left ventricular dysfunction.
This prevent forward blood flow & cause blood back up
into the left atrium & pulmonary vein
Right side heart failure:-
It occur when right ventricle fail to contract effectively .
It causes back up blood to the right atrium & venous
circulation.
PATHOPHYSIOLOGY
• DUE TO ETIOLOGY
• MYOCARDIAL DYSFUNCTION
•
Decrease cardiac output
Decrease systemic blood pressure
Decrease perfusion to kidney
Activation of
baro receptor
Stimulation of vasomotor
regulatory center in
medulaActivation of renin angiotensin aldostiron system
Activation of sympathetic
nervous system
in epinephrin & nor
epinephrine
vasoconstriction
Liver produce angiotensinogen
Renin
In Aldostiron
Sodium & water retainsion
vasoconstriction
Angiotensin-I
Angiotensin-II
vasoconstriction
After load, BP, Heart rate
Ventricular remodeling
Left side heart failure:-
Increase HR:- Due to reduce CO the SNS activate which
increase HR.
Left ventricular hypertrophy
Pulmonary edema.
Nocturia:- In HF there is impair renal function &
decrease urine out put during day but in night fluid move
from interstitial space to back in to the circulatory
system, cardiac work load decrease at night while
resting, these combining effect result in increase renal
blood flow & dieresis.
Pleural effusion
Restlessness
Confusion
Dyspnea:- Due to increase pulmonary pressure
secondary to interstitial & alveolar edema.
Orthopnea
Paroxysmal nocturnal dyspnea:- When patient sleep
there is reabsorption of fluid from dependent body
area when the patient is flat, the patient awakes in a
panic with feeling of suffocation & has strong desire to
sit or stand up.
Right side HF:-
Jugular venous dystenion
Edema in scrotum, pedal, sacrum:-
Weight gain
Skin changes:-Because tissue capillary extraction is
increased in a person with chronic HF the skin may
appear duskey, often lower extremity are shiny &
swellen.
Increase HR.
Asitis
Hepatomegaly
Fatigue:- Due to impaired perfusion to vital organ.
Right upper quadrent pain
Anorexia
Nausea.
Pleural Effusion:- Pleural effusion results from
increasing pressure in the pleural capillaries.
Dysrhythmias:- Chronic heart failure cause
enlargement of chamber of heart which can cause
changes in normal electrical pathway.
Left ventricular thrombus:- The enlarge left ventricle&
decrease CO combine to increase the chance of
thrombus formation in the LV.
Hepatomegaly:- RT ventricle failure cause congestion
with venous blood in liver.
Renal failure:- Decrease CO decrease the perfusion of
kidney which leads to renal insufficiency
History collection
Physical Examination
Serum chemestries, cardiac marker, liver function test,
thyroid function test, CBC, lipid profile
Kidney function test, urine analysis.
Chest x-ray:- To find any structural change.
CT Scan & MRI to detect tissue damage.
12 lead ECG:-To record the electrical activity.
Haemodynamic monitoring
2- diamintional echo
Cardiac chetheterization
Echocardiogram:- To detect how much blood is
pumping.
 Diuretics:- Bumetanide & Fusemide. To remove excessive
fluid.
ACE Inhibitor:-It inhibit potent vasoconstriction and
inhibit sodium retaintion. Ex- Enalpril, Lisinopril &
captopril.
Angiotensin II receptor blockers:- Use with patient who
cannot tolerate ACE inhibitors due to cough or
angioedema. Ex- Losartan & valsartan.
Digitalis:-Positive inotropic agent to increase the heart
ability to pump more effectively by improving contractile
force of the muscle. Ex- Digoxine.
Beta blocker:- To decrease the myocardial work load &
protect against fatal dysrhythmia by blocking
norepinephrine effect of the sympathetic nervous
system. EX- Carvedilol, Metoprolol, bisoprolol.
Aldosterone antagonist:- Aldosterone antagonist
decrease sodium retaintion, sympathetic nervous system
activation & cardiac remodelling.Ex- Spirinolactone &
eplerenone.
Vasodilator:- To decrease the workload of heart by
dilating the peripheral vessels. Ex- Nitroglycerin,
Hydralazine & morphin sulphate.
SURGICAL MANAGEMENT:-
Coronary angioplasty:- To widen blocked or narrow
artery by putting a stent.
CABG:-Here there is removal of blood vessel from
another part of the body and attached against the
blocked vessel.
Implantable cardiac defibrillator:-It is an implantable
cardiac device like a pace maker, wire tunnel through
vein to monitor heart rhythm.
Intra aortic balloon pump:- A small balloon implanted
is inflated inside the aorta when the heart muscle relax.
Before heart muscle pumps the balloon is deflated
helping the blood flow from heart.
Left ventricular assist devise:- These
mechanical device are implanted in to the
abdomen or chest & attached to a weakened
heart to help it pump.
Valve repair or valve replacement surgery:-If
heart fail because of a problematic heart valve,
doctor may want that valve repaired.
Heart transplantation
Assessment:-
Obtain history of symptoms, limits of activity,
response to rest & history of response to drug therapy.
Ask about sleep disturbance, particularly sleep
suddenly intrupped by shortness of breath.
Heartfailure

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Heartfailure

  • 1.
  • 2. Heart failure is an abnormal clinical syndrome that involves inadequate pumping & feeling of heart. (Lewis’s) In heart failure heart is unable to provide sufficient blood to met the oxygen need of the tissue
  • 3. Worldwide 2 crore people are affected by heart failure. Approximately 2% prevalence in developed countries. Women are more survival then man Coronary artery disease is the major cause for HF.
  • 4. The major cause of HF may be divided into two sub groups, those are:- I. Primary cause II. Precipitating cause
  • 5. Coronary artery disease Hypertension Rheumatoid heart disease Congenital heart defect(Ventricular septal defect) Pulmonary hypertension Cardiomyopathy( Viral, substance abuse)
  • 7. Anemia:- In anemia there is decrease o2 carrying capacity of blood which stimulate increase in cardiac output to meet the tissue demand. This leads to increase in cardiac workload & increase in size of LV. Infection:- In infection there is increase in O2 demand of tissue stimulating increase in CO. Thyrotoxicosis:- Change in the tissue metabolic rate,increase HR & workload of the heart. Hypothyroidism:- Indirectly pridispose to Atherosclerosis, severe hypothyroidism decrease myocardial contractility. Dysrhythmia:- May decrease CO and increase wark load & O2 requirment of myocardial tissue.
  • 8. Bacterial Endocardiatis:- It cause increase metabolic demand & O2 requirmentof myocardial tissue. It also cause valve dysfunction which causes stenosis & regurgitation. Pulmonary Emboilism:- Increase pulmonary pressure resulting from obstruction leads to pulmonary hypertension, decrease CO. Pagets Disease:- Increase workload of heart by increase vascular bed in the skeletal muscle. Nutritional Deficiency:- May decrease cardiac function by decrease myocardial muscle mass & myocardial contractility. Hypovolemia:- Increase preload causing volume overload on the right ventricle.
  • 9. II. Right side failure vs left side failure Left side failure:- It results from left ventricular dysfunction. This prevent forward blood flow & cause blood back up into the left atrium & pulmonary vein Right side heart failure:- It occur when right ventricle fail to contract effectively . It causes back up blood to the right atrium & venous circulation.
  • 10. PATHOPHYSIOLOGY • DUE TO ETIOLOGY • MYOCARDIAL DYSFUNCTION • Decrease cardiac output Decrease systemic blood pressure Decrease perfusion to kidney Activation of baro receptor Stimulation of vasomotor regulatory center in medulaActivation of renin angiotensin aldostiron system Activation of sympathetic nervous system in epinephrin & nor epinephrine vasoconstriction Liver produce angiotensinogen Renin In Aldostiron Sodium & water retainsion vasoconstriction Angiotensin-I Angiotensin-II vasoconstriction After load, BP, Heart rate Ventricular remodeling
  • 11. Left side heart failure:- Increase HR:- Due to reduce CO the SNS activate which increase HR. Left ventricular hypertrophy Pulmonary edema. Nocturia:- In HF there is impair renal function & decrease urine out put during day but in night fluid move from interstitial space to back in to the circulatory system, cardiac work load decrease at night while resting, these combining effect result in increase renal blood flow & dieresis.
  • 12. Pleural effusion Restlessness Confusion Dyspnea:- Due to increase pulmonary pressure secondary to interstitial & alveolar edema. Orthopnea Paroxysmal nocturnal dyspnea:- When patient sleep there is reabsorption of fluid from dependent body area when the patient is flat, the patient awakes in a panic with feeling of suffocation & has strong desire to sit or stand up.
  • 13. Right side HF:- Jugular venous dystenion Edema in scrotum, pedal, sacrum:- Weight gain Skin changes:-Because tissue capillary extraction is increased in a person with chronic HF the skin may appear duskey, often lower extremity are shiny & swellen. Increase HR. Asitis Hepatomegaly Fatigue:- Due to impaired perfusion to vital organ. Right upper quadrent pain Anorexia Nausea.
  • 14. Pleural Effusion:- Pleural effusion results from increasing pressure in the pleural capillaries. Dysrhythmias:- Chronic heart failure cause enlargement of chamber of heart which can cause changes in normal electrical pathway. Left ventricular thrombus:- The enlarge left ventricle& decrease CO combine to increase the chance of thrombus formation in the LV. Hepatomegaly:- RT ventricle failure cause congestion with venous blood in liver. Renal failure:- Decrease CO decrease the perfusion of kidney which leads to renal insufficiency
  • 15. History collection Physical Examination Serum chemestries, cardiac marker, liver function test, thyroid function test, CBC, lipid profile Kidney function test, urine analysis. Chest x-ray:- To find any structural change. CT Scan & MRI to detect tissue damage. 12 lead ECG:-To record the electrical activity. Haemodynamic monitoring 2- diamintional echo Cardiac chetheterization Echocardiogram:- To detect how much blood is pumping.
  • 16.  Diuretics:- Bumetanide & Fusemide. To remove excessive fluid. ACE Inhibitor:-It inhibit potent vasoconstriction and inhibit sodium retaintion. Ex- Enalpril, Lisinopril & captopril. Angiotensin II receptor blockers:- Use with patient who cannot tolerate ACE inhibitors due to cough or angioedema. Ex- Losartan & valsartan. Digitalis:-Positive inotropic agent to increase the heart ability to pump more effectively by improving contractile force of the muscle. Ex- Digoxine.
  • 17. Beta blocker:- To decrease the myocardial work load & protect against fatal dysrhythmia by blocking norepinephrine effect of the sympathetic nervous system. EX- Carvedilol, Metoprolol, bisoprolol. Aldosterone antagonist:- Aldosterone antagonist decrease sodium retaintion, sympathetic nervous system activation & cardiac remodelling.Ex- Spirinolactone & eplerenone. Vasodilator:- To decrease the workload of heart by dilating the peripheral vessels. Ex- Nitroglycerin, Hydralazine & morphin sulphate.
  • 18. SURGICAL MANAGEMENT:- Coronary angioplasty:- To widen blocked or narrow artery by putting a stent. CABG:-Here there is removal of blood vessel from another part of the body and attached against the blocked vessel. Implantable cardiac defibrillator:-It is an implantable cardiac device like a pace maker, wire tunnel through vein to monitor heart rhythm. Intra aortic balloon pump:- A small balloon implanted is inflated inside the aorta when the heart muscle relax. Before heart muscle pumps the balloon is deflated helping the blood flow from heart.
  • 19. Left ventricular assist devise:- These mechanical device are implanted in to the abdomen or chest & attached to a weakened heart to help it pump. Valve repair or valve replacement surgery:-If heart fail because of a problematic heart valve, doctor may want that valve repaired. Heart transplantation
  • 20. Assessment:- Obtain history of symptoms, limits of activity, response to rest & history of response to drug therapy. Ask about sleep disturbance, particularly sleep suddenly intrupped by shortness of breath.