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CONGESTIVE HEART
FAILURE
By :-
Baljinder Singh
M.sc (MSN)
C H F
 Definition: It is a clinical syndrome
resulting from the inability of heart
to pump enough blood at rest or
during exercise even though the
filling pressures are adequate.
Incidence
 Major public health problem in
industrialized countries.
 Common in elderly.
Etiology
 Divided in to 3 subgroups
-Abnormal loading conditions
-Abnormal muscle function
-Precipitating factors
Etiology (contd..)
 Abnormal loading conditions
Increased preload
Refers to the length of the ventricular
myocardial fibers just before ventricular
contraction and EDV
-Valvular regurgitation
-Hypervolemia
-Congenital diseases
(ASD,VSD,PDA)
Etiology (contd..)
 Increased after load
Correspond to the amount of intra
myocardial wall tension that the heart
must generate to overcome systolic
pressure and allows ventricular emptying.
-Aortic valvular stenosis
-pulmonary valve stenosis
-Systemic and pulmonary hypertension
-Increased PVR
-Increased blood viscosity
Etiology (contd.)
 Abnormal muscle function
-Conditions that interfere with myocardial
contractibility
MI
Myocarditis
Cardiomyopathy
ventricular aneurism
-External compression
(constrictive pericarditis,cardiac
tamponade)
Precipitating factors
 Physical and emotional stress
 Dysrrhythmias
 Infection
 Anemia
 Thyroid disorders
 Pregnancy
 Paget disease
 Nutritional deficiency
 Pulmonary diseases
 Hypervolemia
Pathophysiology
Diseased Normal
myocardium myocardium
Unable to meet the demands
Activation of compensatory system
(sympathetic stimulation)
Fails
Increased residual volume in left
ventricle
Pathophysiology (contd..)
Decreased ability to receive blood
from left atrium
Left atrium work hard to eject blood
dilation and hypertrophy
Pulmonary edema and congestion
Pathophysiology (contd…)
Increased pressure in pulmonary
vascular system
Right ventricular dilation&hypertrophy
Fails
Engorgement of systemic venous
system
Congestion in GIT,Liver
viscera,Kidneys,Legs,sacrum
Pathophysiology (contd..)
Conditions that causes RVF
- Pulmonary diseases
(PAH,Pulmonary embolism,COPD,cor
pulmonale)
-Constrictive Pericarditis
-Tricuspid and pulmonary valvular
disorders
-RV infarction
Pathophysiology (contd..)
 Cardiac reserve (Hearts ability to
increase the output in response to
stress(5 the times the normal)
 But in the diseased heart, it fails to
respond to body’s increased
demands
 Compensatory mechanism will be
initiated
Pathophysiology contd..
 Compensatory mechanisms are
-Ventricular dilation: Lengthening of
the muscle fibers Increased
volume of heart chambers
Increased preload and cardiac out
put leads to reduced contractibility
when stretched beyond capacity
Increased oxygen demand
hypoxia
Pathophysiology (contd..)
 Ventricular hypertrophy-Increase in
the diameter of muscle fibers
Size and weight of heart increases
Increased oxygen demand
Hypoxia and reduced contractibility
Pathophysiology(contd..)
 Increased sympathetic stimulation
Increased heart rate and peripheral
vascular resistance
Reduced renal flow and increased
renal conservation of water and
sodium
Fluid overload and increased workload
Forms of heart failure
 Systolic versus diastolic failure
Systolic-Inability to contract normally
Diastolic-Inability to relax or fill normally
 High output versus low output
Low output-IHD,
HT,cardiomyopathy,pericardial diseases
Highoutput-
Hyperthyroidism,anemia,pregnancy,paget
disease
Forms (contd..)
 Acute versus chronic
Acute –Acute large MI
Chronic-Dilated cardiomyopathy
multivalvular heart disease
 Right sided versus left sided
RVF-PAH,Pulmonary
stenosis,pulmonary embolism,
LVF-Aortic stenosis,Post MI
Types (contd..)
 Backward versus forward H F
backward-ventricles fail to fill
normally Increased pressure in
the atrium and venous system
sodium and water retention edema
Forward-Inadequate discharge of
blood in to the arterial system
Clinical features
 LVF-Dyspnea(PND)
Orthopnea
cough(frothy&blood tinged
sputum)
chyne stoke respiration
pulmonary edema (extreme
breathlessness,anxiety,frothy
sputum, nasal flarring)
C/F Contd
 Cardiovascular signs –
Enlarged left laterally displaced
apical impulse, Heart gallop(S3 & S4)
pulses alternas
 Cerebral hypoxia-
Anxiety,Irritability,Restlesness,confu
sion,Impaired memory, Insomnia
 Renal changes-Oliguria,fatigue and
muscular weakness
C/F Contd
 RVF-Peripherl edema and venous
congestion,
Hepatomegaly and abdominal pain
Cardiac cirrhosis and ascitis
Anorexia,nausea and bloating
cardiac cachexia
Pitting edema
Jugular vein distention, Increased CVP
Anxiety and depression
Complications
 Acute pulmonary edema
 Refractory heart failure
Diagnosis
 PND
 Neck vein distention
 Cardiomegaly
 Pulmonary edema
 Gallop
 Increased CV
 Hepatojugular reflex
Framingham criteria
Major criteria Minor criteria
 Peripheral edema
 Night cough
 Dyspnea on exertion
 Pleural effusion
 Hepatomegaley
 Reduced vital capacity
 Tachycardia(>120bpm)
Presence of one major or 2 minor criteria confirms the diagnosis
Diagnosis(contd..)
 Chest radiography
 ABG analysis
 Liver enzymes
 BUN and creatinine
 ECG
Medical management
 Removal of precipitating factors
 Correction of underlying causes
 Prevention of deterioration of cardiac
function
 Control of CHF state
Immediate management
 Positioning – high fowlers position
 0xygen administration(8–10 Lts,)
Management contd
 Digitalis-Increses ventricular emptying,
slow conduction of impulses through AV
node, Increases stroke volume and
cardiac output
-effective in systolic heart failure
-0.25 6 hourly for adults, for elderly o.125
mg 6 hourly
-Reduce dose in renal impairement
-Should not be given in heart failure with
high output
-Digitalis toxicity should be monitered
Management contd
 Dopamine and dobutamine
Low output failure
Dopamine-2-10 microgram/kg/mt
Dobutamine-2.5-10 microgram/kg/mt
 Anticoagulants
 Antiarrythmics
 ACEI
 Aldosterone antagonist;spironolactone25mg /day
 Beta adrenergic blockers
CHF: Diuretics
 Reduce volume overload
 Reduce sodium overload
 Preload reduction
Diuretics
Thiazide Diuretics
 Chlorthalidone
 Metolazone
Loop Diuretics
 Furosemide
 Torsemide
Potassium Sparing
Diuretics
 Spironolactone
 Amiloride
CHF: ACE Inhibitors
 Improve hemodynamic status
 Improve symptoms
 Reduce incidence of hospitization
 Slow progression of disease
 Reduce mortality
ACE Inhibitors
 Captopril
 Enalapril
 Lisinopril
 Quinapril
 Trandolapril
 Fosinopril
Management contd
 Reduction of cardiac workload
Reducing the physical activity
Emotional rest and reduction of
anxiety
Diet: sodium 1 gm / day
Water 1000 ml / day
potassium supplements
vasodilators – sodium nitroprusside and
Isosorbid dinitrate
 Aminophylline 240- 480 mg IV
Surgical management
 Surgical correction of valvular disorders
 Heart transplantation
 Cardiopulmonary bypass
 Intra aortic balloon pump
Nursing management
 Impaired gas exchange related to to fluid
in the alveoli
 Decreased cardiac output related to heart
failure and Dysrrhythmias
 Fluid volume excess related to reduced
cardiac output and Na and water retention
 Decreased peripheral tissue perfusion
related to reduced cardiac output
 Activity intolerance related to reduced
cardiac output
Nursing management
 High risk for impaired skin integrity
related to reduced peripheral tissue
perfusion
 High risk for digitalis toxicity related
to impaired excretion
 Anxiety and fear of death related to
reduced cardiac output and hypoxia
Congestive Heart Failure

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Congestive Heart Failure

  • 2. C H F  Definition: It is a clinical syndrome resulting from the inability of heart to pump enough blood at rest or during exercise even though the filling pressures are adequate.
  • 3. Incidence  Major public health problem in industrialized countries.  Common in elderly.
  • 4. Etiology  Divided in to 3 subgroups -Abnormal loading conditions -Abnormal muscle function -Precipitating factors
  • 5. Etiology (contd..)  Abnormal loading conditions Increased preload Refers to the length of the ventricular myocardial fibers just before ventricular contraction and EDV -Valvular regurgitation -Hypervolemia -Congenital diseases (ASD,VSD,PDA)
  • 6. Etiology (contd..)  Increased after load Correspond to the amount of intra myocardial wall tension that the heart must generate to overcome systolic pressure and allows ventricular emptying. -Aortic valvular stenosis -pulmonary valve stenosis -Systemic and pulmonary hypertension -Increased PVR -Increased blood viscosity
  • 7. Etiology (contd.)  Abnormal muscle function -Conditions that interfere with myocardial contractibility MI Myocarditis Cardiomyopathy ventricular aneurism -External compression (constrictive pericarditis,cardiac tamponade)
  • 8. Precipitating factors  Physical and emotional stress  Dysrrhythmias  Infection  Anemia  Thyroid disorders  Pregnancy  Paget disease  Nutritional deficiency  Pulmonary diseases  Hypervolemia
  • 9. Pathophysiology Diseased Normal myocardium myocardium Unable to meet the demands Activation of compensatory system (sympathetic stimulation) Fails Increased residual volume in left ventricle
  • 10. Pathophysiology (contd..) Decreased ability to receive blood from left atrium Left atrium work hard to eject blood dilation and hypertrophy Pulmonary edema and congestion
  • 11. Pathophysiology (contd…) Increased pressure in pulmonary vascular system Right ventricular dilation&hypertrophy Fails Engorgement of systemic venous system Congestion in GIT,Liver viscera,Kidneys,Legs,sacrum
  • 12. Pathophysiology (contd..) Conditions that causes RVF - Pulmonary diseases (PAH,Pulmonary embolism,COPD,cor pulmonale) -Constrictive Pericarditis -Tricuspid and pulmonary valvular disorders -RV infarction
  • 13. Pathophysiology (contd..)  Cardiac reserve (Hearts ability to increase the output in response to stress(5 the times the normal)  But in the diseased heart, it fails to respond to body’s increased demands  Compensatory mechanism will be initiated
  • 14. Pathophysiology contd..  Compensatory mechanisms are -Ventricular dilation: Lengthening of the muscle fibers Increased volume of heart chambers Increased preload and cardiac out put leads to reduced contractibility when stretched beyond capacity Increased oxygen demand hypoxia
  • 15. Pathophysiology (contd..)  Ventricular hypertrophy-Increase in the diameter of muscle fibers Size and weight of heart increases Increased oxygen demand Hypoxia and reduced contractibility
  • 16. Pathophysiology(contd..)  Increased sympathetic stimulation Increased heart rate and peripheral vascular resistance Reduced renal flow and increased renal conservation of water and sodium Fluid overload and increased workload
  • 17. Forms of heart failure  Systolic versus diastolic failure Systolic-Inability to contract normally Diastolic-Inability to relax or fill normally  High output versus low output Low output-IHD, HT,cardiomyopathy,pericardial diseases Highoutput- Hyperthyroidism,anemia,pregnancy,paget disease
  • 18. Forms (contd..)  Acute versus chronic Acute –Acute large MI Chronic-Dilated cardiomyopathy multivalvular heart disease  Right sided versus left sided RVF-PAH,Pulmonary stenosis,pulmonary embolism, LVF-Aortic stenosis,Post MI
  • 19. Types (contd..)  Backward versus forward H F backward-ventricles fail to fill normally Increased pressure in the atrium and venous system sodium and water retention edema Forward-Inadequate discharge of blood in to the arterial system
  • 20. Clinical features  LVF-Dyspnea(PND) Orthopnea cough(frothy&blood tinged sputum) chyne stoke respiration pulmonary edema (extreme breathlessness,anxiety,frothy sputum, nasal flarring)
  • 21. C/F Contd  Cardiovascular signs – Enlarged left laterally displaced apical impulse, Heart gallop(S3 & S4) pulses alternas  Cerebral hypoxia- Anxiety,Irritability,Restlesness,confu sion,Impaired memory, Insomnia  Renal changes-Oliguria,fatigue and muscular weakness
  • 22. C/F Contd  RVF-Peripherl edema and venous congestion, Hepatomegaly and abdominal pain Cardiac cirrhosis and ascitis Anorexia,nausea and bloating cardiac cachexia Pitting edema Jugular vein distention, Increased CVP Anxiety and depression
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  • 26. Complications  Acute pulmonary edema  Refractory heart failure
  • 27. Diagnosis  PND  Neck vein distention  Cardiomegaly  Pulmonary edema  Gallop  Increased CV  Hepatojugular reflex Framingham criteria Major criteria Minor criteria  Peripheral edema  Night cough  Dyspnea on exertion  Pleural effusion  Hepatomegaley  Reduced vital capacity  Tachycardia(>120bpm) Presence of one major or 2 minor criteria confirms the diagnosis
  • 28. Diagnosis(contd..)  Chest radiography  ABG analysis  Liver enzymes  BUN and creatinine  ECG
  • 29. Medical management  Removal of precipitating factors  Correction of underlying causes  Prevention of deterioration of cardiac function  Control of CHF state
  • 30. Immediate management  Positioning – high fowlers position  0xygen administration(8–10 Lts,)
  • 31. Management contd  Digitalis-Increses ventricular emptying, slow conduction of impulses through AV node, Increases stroke volume and cardiac output -effective in systolic heart failure -0.25 6 hourly for adults, for elderly o.125 mg 6 hourly -Reduce dose in renal impairement -Should not be given in heart failure with high output -Digitalis toxicity should be monitered
  • 32. Management contd  Dopamine and dobutamine Low output failure Dopamine-2-10 microgram/kg/mt Dobutamine-2.5-10 microgram/kg/mt  Anticoagulants  Antiarrythmics  ACEI  Aldosterone antagonist;spironolactone25mg /day  Beta adrenergic blockers
  • 33. CHF: Diuretics  Reduce volume overload  Reduce sodium overload  Preload reduction
  • 34. Diuretics Thiazide Diuretics  Chlorthalidone  Metolazone Loop Diuretics  Furosemide  Torsemide Potassium Sparing Diuretics  Spironolactone  Amiloride
  • 35. CHF: ACE Inhibitors  Improve hemodynamic status  Improve symptoms  Reduce incidence of hospitization  Slow progression of disease  Reduce mortality
  • 36. ACE Inhibitors  Captopril  Enalapril  Lisinopril  Quinapril  Trandolapril  Fosinopril
  • 37. Management contd  Reduction of cardiac workload Reducing the physical activity Emotional rest and reduction of anxiety Diet: sodium 1 gm / day Water 1000 ml / day potassium supplements vasodilators – sodium nitroprusside and Isosorbid dinitrate  Aminophylline 240- 480 mg IV
  • 38. Surgical management  Surgical correction of valvular disorders  Heart transplantation  Cardiopulmonary bypass  Intra aortic balloon pump
  • 39. Nursing management  Impaired gas exchange related to to fluid in the alveoli  Decreased cardiac output related to heart failure and Dysrrhythmias  Fluid volume excess related to reduced cardiac output and Na and water retention  Decreased peripheral tissue perfusion related to reduced cardiac output  Activity intolerance related to reduced cardiac output
  • 40. Nursing management  High risk for impaired skin integrity related to reduced peripheral tissue perfusion  High risk for digitalis toxicity related to impaired excretion  Anxiety and fear of death related to reduced cardiac output and hypoxia