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HEART FAILURE
Dr. Sameh Ahmad Muhamad abdelghany
Lecturer Of Clinical Pharmacology
Mansura Faculty of medicine
2
Introduction
Causes & Types
Pathophysiology &
risk fators
Diagnosis
Treatment
CONTENTS
INTRODUCTION
4
Introduction
 Definiton:
 A clinical syndrome resulting from any structural or
functional cardiac defect
 The heart is unable to pump sufficiently to maintain blood
flow to meet the body's needs
5
Introduction
 The most common causes of heart failure are
coronary artery disease, high blood pressure, and
diabetes.
 HF is diagnosed on the presence of characteristic
signs and symptoms and not on the basis of any
diagnostic tests
6
Introduction
 Heart failure is a common, costly, and potentially fatal
condition.
 In 2015 it affected about 40 million people globally.
 Overall around 2% of adults have heart failure and in those
over the age of 65, this increases to 6–10%.
 In the year after diagnosis the risk of death is about 35%
after which it decreases to below 10% each year.
CAUSES & TYPES
8
Common causes of HF
 Ischemic heart disease ~ 40 percent
 Dilated cardiomyopathy ~ 30 percent
 Primary valvular heart disease ~ 15
percent
 Hypertensive heart disease ~ 10 percent
 Other ~ 5 percent
9
Types of HF
 According to cardiac output:
a. Low-Output Heart Failure
b. High-Output Heart Failure
 According to anatomical side
a. Left side heart failure
b. Right side heart failure
 According to onset
a. Acute heart failure
b. Chronic heart failure
10
Low-Output HF
 Causes:
I. Systolic Dysfunction
 Coronary Artery Disease
 Idiopathic dilated cardiomyopathy (DCM)
 Hypertension
 Valvular Heart Disease
11
Low-Output HF
II. Diastolic Dysfunction
 Hypertension
 Coronary artery disease
 Hypertrophic obstructive cardiomyopathy (HCM)
 Restrictive cardiomyopathy
12
High-Output HF
 Seen with hyperthyroidism, beri-beri, carcinoid,
anemia
 Often with normal cardiac output
PATHOPHYSIOLOGY
14
Pathophysiology of HF
 Pump fails → decreased stroke volume /CO.
 Compensatory mechanisms kick in to increase CO
 SNS stimulation → release of epinephrine/nor-
epinephrine
o Increase HR
o Increase contractility
o Peripheral vasoconstriction (increases afterload)
 Myocardial hypertrophy: walls of heart thicken to
provide more muscle mass → stronger contractions
15
Pathophysiology of HF
 Hormonal response:
 ↓ renal perfusion interpreted by juxtaglomerular
apparatus as hypovolemia. Thus: Kidneys release
renin, which stimulates conversion of antiotensin I →
angiotensin II, which causes:
o Aldosterone release → Na retention and water
retention (via ADH secretion)
o Peripheral vasoconstriction
16
Pathophysiology of HF
 Compensatory mechanisms may restore CO to near-
normal.
 But, if excessive the compensatory mechanisms can
worsen heart failure because:
 Vasoconstriction:
o ↑ the resistance against which heart has to pump (i.e.,
↑ afterload), and may therefore ↓ CO
17
Pathophysiology of HF
 Na and water retention:
o ↑ fluid volume, which ↑ preload. If too much
“stretch” (d/t too much fluid) → ↓ strength of
contraction and ↓ CO
 Excessive tachycardia → ↓ diastolic filling time →
↓ventricular filling → ↓ SV and CO
18
Pathophysiology of HF
RISK FACTORS
20
Risk factors of HF
 CAD
 Age
 HTN
 Obesity
 Cigarette smoking
 Diabetes mellitus
 High cholesterol
 African descent
DIAGNOSIS
22
C/P of HF
 Symptoms
 Left Heart Failure:
o Dyspnea on exertion
o Dyspnea at rest
o Orthpnea
o Paroxysmal nocturnal dyspnea (PND)
o Fatigue, inability to exercise
23
C/P of HF
 Symptoms
 Right Heart Failure:
o Swelling of feet, hands
o Abdominal distention/fullness
o Right upper quadrant pain
o Early satiety
o Weight loss (cardiac cachexia)
24
C/P of HF
 Signs
 Left Heart Failure:
o Rales
o Pleural effusions
o Displaced apical impulse
o Tachycardia, LVS3, murmur of MR(mitral regurge)
o Narrow pulse pressure
25
C/P of HF
 Signs
 Right Heart Failure:
o Edema of lower extremities
o Elevated JVP(jugular vein pressure)/+
HJR(hepatojugular reflux)
o RVS3, murmur of TR(tricuspid regurge)
o Hepatomegaly, RUQ(right upper quadrant) tenderness
o Ascites - Pleural effusions
26
C/P of HF
27
Classification of HF
 New York Heart Association (NYHA)
 Class I : symptoms of HF only at levels that would
limit normal individuals.
 Class II : symptoms of HF with ordinary exertion
 Class III : symptoms of HF on less than ordinary
exertion
 Class IV : symptoms of HF at rest
28
Classification of HF
 American College of Cardiology and the American
Heart Association(ACC/AHA) Guidelines
 Stage A : High risk of HF, without structural heart
disease or symptoms
 Stage B : Heart disease with asymptomatic left
ventricular dysfunction
 Stage C : Prior or current symptoms of HF
 Stage D : Advanced heart disease and severely
symptomatic or refractory HF
29
Clinical Presentation of HF
30
Investigation
I. LAB
A) Non specific
 CBC(Since anemia can exacerbate heart failure)
 Serum electrolytes and creatinine( before starting high
dose diuretics)
 Fasting Blood glucose(To evaluate for possible diabetes
mellitus)
 Thyroid function tests
 Viral studies (If viral myocarditis suspected)
 Others
31
Investigation
I. LAB
B) Specific
 BNP:
o With chronic heart failure, atrial myocytes secrete
increase amounts of atrial natriuretic peptide (ANP) and
brain natriuretic peptide (BNP) in response to high atrial
and ventricular filling pressures
o Promotes vasodilation, diuresis and natriuresis
o Usually is > 400 pg/mL in patients with dyspnea due to
heart failure.
32
Investigation
II. Radiological
 Chest X-ray:
o Cardiomegaly
o Cephalization of the
pulmonary vessels
o Kerley B-lines
o Pleural effusions
33
Investigation
Cardiomegaly
Pulmonary
vessel
congestion
Kerley B lines
34
Investigation
III. Cardiac testing
 ECG:
o May show specific cause of heart failure e.g Ischemic
heart disease
 ECHO:
o Left ventricular ejection fraction
o Structural/valvular abnormalities
35
Investigation
III. Cardiac testing
 Exercise Testing
o Should be part of initial evaluation of all patients with
CHF.
 Coronary arteriography
o Should be performed in patients presenting with heart
failure who have angina or significant ischemia
o Measure cardiac output, degree of left ventricular
dysfunction, and left ventricular end-diastolic pressure.
36
Diagnosis of HF
 HF should be suspected on the basis of clinical
presentation and radiographic findings.
 It’s a clinical diagnosis. There is no diagnostic test!
 Depressed ventricular EF should be confirmed with
echocardiography, or cardiac catheterization with left
ventriculography.
TREATMENT
38
Treatment
Management of Chronic heart failure:
 General measures
 Correct underlying cause
 Remove precipitating cause
 Prevention of deterioration of cardiac function
 Control of congestive HF state
39
Treatment
Correction of systemic factors
 Thyroid dysfunction
 Infections
 Uncontrolled diabetes
 Hypertension
40
Treatment
Nonpharmacologic therapy:
 Exercise training:
o for stable HF patients increased exercise capacity,
decreased hospitalization rate, increased quality
of life, decreased symptoms.
 Weight loss in obese patients
 Dietary Na restriction
41
Treatment
Nonpharmacologic therapy:
 Fluid and free water restriction especially if
hyponatremic
 Minimize medications known to have deleterious
effects on heart failure (negative inotrops, NSAIDs,
over-the-counter stimulants)
 Oxygen
 Fluid removal (dialysis, thoracentesis, paracentesis)
42
Medical Treatment
Order of drug therapy
o Loop diuretics
o ACE inhibitor (or ARB if not tolerated)
o Beta blockers
o Digoxin
o Hydralazine, Nitrate
o Potassium sparing diuretics
43
Medical Treatment
Diuretics
A. Loop diuretics
 Furosemide, buteminide
 For Fluid control, and to help relieve symptoms
B. Potassium-sparing diuretics
 Spironolactone, eplerenone
 Help enhance diuresis
 Maintain potassium
 Shown to improve survival in CHF
44
Medical Treatment
ACE Inhibitor
 Improve survival in patients with all severities of heart
failure.
 Begin therapy low and titrate up as possible:
o Enalapril
o Captopril
o Lisinopril
 If cannot tolerate, may try ARB
45
Medical Treatment
Beta Blocker therapy
 Certain Beta blockers (carvedilol, metoprolol,
bisoprolol) can improve overall survival in NYHA
class II to III HF, probably in class IV.
 Contraindicated:
o Heart rate <60 bpm
o Symptomatic bradycardia
o Signs of peripheral hypoperfusion
o COPD, asthma
o Prolonged PR interval, 2nd or 3rd degree heart block
46
Medical Treatment
Hydralazine plus Nitrates
 Hydralazine + Isosorbide dinitrate
 can be useful to reduce morbidity or mortality in
patients with current or prior symptomatic HF who
cannot be given an ACE inhibitor or ARB
 Recommended for African Americans with NYHA
class III–IV
 Decreased mortality, lower rates of hospitalization, and
improvement in quality of life.
47
Medical Treatment
Digoxin
 Given to patients with HF to control symptoms such as
fatigue, dyspnea, exercise intolerance
 Digoxin can be used in HF patients with atrial
fibrillation to help rate control
 Shown to significantly reduce hospitalization for heart
failure, but no benefit in terms of overall mortality.
48
Medical Treatment
Other important medication
 Statin therapy:
 recommended in CHF for the secondary prevention of
cardiovascular disease.
 Benefits:
o Improved LVEF(left ventricular ejection fraction)
o Reversal of ventricular remodeling
o Reduction in inflammatory markers e.g CRP
49
Medical Treatment
Meds to AVOID in heart failure
 NSAIDS
o Can cause worsening of pre-existing HF
 Thiazolidinediones
o Cause fluid retention that can exacerbate HF
 Metformin
o increased risk of potentially lactic acidosis
50
Implantable Cardioverter-
Defibrillators for HF
 Sustained ventricular
tachycardia is
associated with sudden
cardiac death in HF.
 About one-third of
mortality in HF is due
to sudden cardiac
death.
ACUTE HEART
FAILURE
52
Acute Decompensated HF
 Cardiogenic pulmonary edema is a common and
sometimes fatal cause of acute respiratory distress.
 Characterized by the transudation of excess fluid into
the lungs secondary to an increase in left atrial and
subsequently pulmonary venous and pulmonary
capillary pressures.
53
Acute Decompensated HF
 Causes:
 Acute MI
o Rupture of chordae tendinae/acute mitral valve
insufficiency
 Volume Overload
o Transfusions, IV fluids
o Non-compliance with diuretics, diet (high salt intake)
 Worsening valvular defect
o Aortic stenosis
54
Acute Decompensated HF
 Clinical manifestations:
 Symptoms
o Severe dyspnea
o Cough
55
Acute Decompensated HF
 Clinical manifestations:
 Signs
o Tachypnea
o Tachycardia
o Hypertension/Hypotension
o Crackles on lung exam
o Increased JVD(jagular venous distension)
o S3, S4 or new murmur
56
Acute Decompensated HF
 Investigations:
 Chemistry, CBC
 ECG
 Chest X-ray
 May consider cardiac enzymes
 2D-Echo
57
Acute Decompensated HF
 Treatment
 Oxygen, mechanical ventilation if needed
 Loop diuretics (Lasix)
 Morphine
 Vasodilator therapy (nitroglycerin)
 Positive inotropes e.g Dobutmaine
 Nesiritide (BNP) : can help in acute setting, for
short term therapy
58
Acute Decompensated HF
59
thanks
F o r W a t c h i n g

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heartfailure-181102160805.pdf

  • 1. HEART FAILURE Dr. Sameh Ahmad Muhamad abdelghany Lecturer Of Clinical Pharmacology Mansura Faculty of medicine
  • 2. 2 Introduction Causes & Types Pathophysiology & risk fators Diagnosis Treatment CONTENTS
  • 4. 4 Introduction  Definiton:  A clinical syndrome resulting from any structural or functional cardiac defect  The heart is unable to pump sufficiently to maintain blood flow to meet the body's needs
  • 5. 5 Introduction  The most common causes of heart failure are coronary artery disease, high blood pressure, and diabetes.  HF is diagnosed on the presence of characteristic signs and symptoms and not on the basis of any diagnostic tests
  • 6. 6 Introduction  Heart failure is a common, costly, and potentially fatal condition.  In 2015 it affected about 40 million people globally.  Overall around 2% of adults have heart failure and in those over the age of 65, this increases to 6–10%.  In the year after diagnosis the risk of death is about 35% after which it decreases to below 10% each year.
  • 8. 8 Common causes of HF  Ischemic heart disease ~ 40 percent  Dilated cardiomyopathy ~ 30 percent  Primary valvular heart disease ~ 15 percent  Hypertensive heart disease ~ 10 percent  Other ~ 5 percent
  • 9. 9 Types of HF  According to cardiac output: a. Low-Output Heart Failure b. High-Output Heart Failure  According to anatomical side a. Left side heart failure b. Right side heart failure  According to onset a. Acute heart failure b. Chronic heart failure
  • 10. 10 Low-Output HF  Causes: I. Systolic Dysfunction  Coronary Artery Disease  Idiopathic dilated cardiomyopathy (DCM)  Hypertension  Valvular Heart Disease
  • 11. 11 Low-Output HF II. Diastolic Dysfunction  Hypertension  Coronary artery disease  Hypertrophic obstructive cardiomyopathy (HCM)  Restrictive cardiomyopathy
  • 12. 12 High-Output HF  Seen with hyperthyroidism, beri-beri, carcinoid, anemia  Often with normal cardiac output
  • 14. 14 Pathophysiology of HF  Pump fails → decreased stroke volume /CO.  Compensatory mechanisms kick in to increase CO  SNS stimulation → release of epinephrine/nor- epinephrine o Increase HR o Increase contractility o Peripheral vasoconstriction (increases afterload)  Myocardial hypertrophy: walls of heart thicken to provide more muscle mass → stronger contractions
  • 15. 15 Pathophysiology of HF  Hormonal response:  ↓ renal perfusion interpreted by juxtaglomerular apparatus as hypovolemia. Thus: Kidneys release renin, which stimulates conversion of antiotensin I → angiotensin II, which causes: o Aldosterone release → Na retention and water retention (via ADH secretion) o Peripheral vasoconstriction
  • 16. 16 Pathophysiology of HF  Compensatory mechanisms may restore CO to near- normal.  But, if excessive the compensatory mechanisms can worsen heart failure because:  Vasoconstriction: o ↑ the resistance against which heart has to pump (i.e., ↑ afterload), and may therefore ↓ CO
  • 17. 17 Pathophysiology of HF  Na and water retention: o ↑ fluid volume, which ↑ preload. If too much “stretch” (d/t too much fluid) → ↓ strength of contraction and ↓ CO  Excessive tachycardia → ↓ diastolic filling time → ↓ventricular filling → ↓ SV and CO
  • 20. 20 Risk factors of HF  CAD  Age  HTN  Obesity  Cigarette smoking  Diabetes mellitus  High cholesterol  African descent
  • 22. 22 C/P of HF  Symptoms  Left Heart Failure: o Dyspnea on exertion o Dyspnea at rest o Orthpnea o Paroxysmal nocturnal dyspnea (PND) o Fatigue, inability to exercise
  • 23. 23 C/P of HF  Symptoms  Right Heart Failure: o Swelling of feet, hands o Abdominal distention/fullness o Right upper quadrant pain o Early satiety o Weight loss (cardiac cachexia)
  • 24. 24 C/P of HF  Signs  Left Heart Failure: o Rales o Pleural effusions o Displaced apical impulse o Tachycardia, LVS3, murmur of MR(mitral regurge) o Narrow pulse pressure
  • 25. 25 C/P of HF  Signs  Right Heart Failure: o Edema of lower extremities o Elevated JVP(jugular vein pressure)/+ HJR(hepatojugular reflux) o RVS3, murmur of TR(tricuspid regurge) o Hepatomegaly, RUQ(right upper quadrant) tenderness o Ascites - Pleural effusions
  • 27. 27 Classification of HF  New York Heart Association (NYHA)  Class I : symptoms of HF only at levels that would limit normal individuals.  Class II : symptoms of HF with ordinary exertion  Class III : symptoms of HF on less than ordinary exertion  Class IV : symptoms of HF at rest
  • 28. 28 Classification of HF  American College of Cardiology and the American Heart Association(ACC/AHA) Guidelines  Stage A : High risk of HF, without structural heart disease or symptoms  Stage B : Heart disease with asymptomatic left ventricular dysfunction  Stage C : Prior or current symptoms of HF  Stage D : Advanced heart disease and severely symptomatic or refractory HF
  • 30. 30 Investigation I. LAB A) Non specific  CBC(Since anemia can exacerbate heart failure)  Serum electrolytes and creatinine( before starting high dose diuretics)  Fasting Blood glucose(To evaluate for possible diabetes mellitus)  Thyroid function tests  Viral studies (If viral myocarditis suspected)  Others
  • 31. 31 Investigation I. LAB B) Specific  BNP: o With chronic heart failure, atrial myocytes secrete increase amounts of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) in response to high atrial and ventricular filling pressures o Promotes vasodilation, diuresis and natriuresis o Usually is > 400 pg/mL in patients with dyspnea due to heart failure.
  • 32. 32 Investigation II. Radiological  Chest X-ray: o Cardiomegaly o Cephalization of the pulmonary vessels o Kerley B-lines o Pleural effusions
  • 34. 34 Investigation III. Cardiac testing  ECG: o May show specific cause of heart failure e.g Ischemic heart disease  ECHO: o Left ventricular ejection fraction o Structural/valvular abnormalities
  • 35. 35 Investigation III. Cardiac testing  Exercise Testing o Should be part of initial evaluation of all patients with CHF.  Coronary arteriography o Should be performed in patients presenting with heart failure who have angina or significant ischemia o Measure cardiac output, degree of left ventricular dysfunction, and left ventricular end-diastolic pressure.
  • 36. 36 Diagnosis of HF  HF should be suspected on the basis of clinical presentation and radiographic findings.  It’s a clinical diagnosis. There is no diagnostic test!  Depressed ventricular EF should be confirmed with echocardiography, or cardiac catheterization with left ventriculography.
  • 38. 38 Treatment Management of Chronic heart failure:  General measures  Correct underlying cause  Remove precipitating cause  Prevention of deterioration of cardiac function  Control of congestive HF state
  • 39. 39 Treatment Correction of systemic factors  Thyroid dysfunction  Infections  Uncontrolled diabetes  Hypertension
  • 40. 40 Treatment Nonpharmacologic therapy:  Exercise training: o for stable HF patients increased exercise capacity, decreased hospitalization rate, increased quality of life, decreased symptoms.  Weight loss in obese patients  Dietary Na restriction
  • 41. 41 Treatment Nonpharmacologic therapy:  Fluid and free water restriction especially if hyponatremic  Minimize medications known to have deleterious effects on heart failure (negative inotrops, NSAIDs, over-the-counter stimulants)  Oxygen  Fluid removal (dialysis, thoracentesis, paracentesis)
  • 42. 42 Medical Treatment Order of drug therapy o Loop diuretics o ACE inhibitor (or ARB if not tolerated) o Beta blockers o Digoxin o Hydralazine, Nitrate o Potassium sparing diuretics
  • 43. 43 Medical Treatment Diuretics A. Loop diuretics  Furosemide, buteminide  For Fluid control, and to help relieve symptoms B. Potassium-sparing diuretics  Spironolactone, eplerenone  Help enhance diuresis  Maintain potassium  Shown to improve survival in CHF
  • 44. 44 Medical Treatment ACE Inhibitor  Improve survival in patients with all severities of heart failure.  Begin therapy low and titrate up as possible: o Enalapril o Captopril o Lisinopril  If cannot tolerate, may try ARB
  • 45. 45 Medical Treatment Beta Blocker therapy  Certain Beta blockers (carvedilol, metoprolol, bisoprolol) can improve overall survival in NYHA class II to III HF, probably in class IV.  Contraindicated: o Heart rate <60 bpm o Symptomatic bradycardia o Signs of peripheral hypoperfusion o COPD, asthma o Prolonged PR interval, 2nd or 3rd degree heart block
  • 46. 46 Medical Treatment Hydralazine plus Nitrates  Hydralazine + Isosorbide dinitrate  can be useful to reduce morbidity or mortality in patients with current or prior symptomatic HF who cannot be given an ACE inhibitor or ARB  Recommended for African Americans with NYHA class III–IV  Decreased mortality, lower rates of hospitalization, and improvement in quality of life.
  • 47. 47 Medical Treatment Digoxin  Given to patients with HF to control symptoms such as fatigue, dyspnea, exercise intolerance  Digoxin can be used in HF patients with atrial fibrillation to help rate control  Shown to significantly reduce hospitalization for heart failure, but no benefit in terms of overall mortality.
  • 48. 48 Medical Treatment Other important medication  Statin therapy:  recommended in CHF for the secondary prevention of cardiovascular disease.  Benefits: o Improved LVEF(left ventricular ejection fraction) o Reversal of ventricular remodeling o Reduction in inflammatory markers e.g CRP
  • 49. 49 Medical Treatment Meds to AVOID in heart failure  NSAIDS o Can cause worsening of pre-existing HF  Thiazolidinediones o Cause fluid retention that can exacerbate HF  Metformin o increased risk of potentially lactic acidosis
  • 50. 50 Implantable Cardioverter- Defibrillators for HF  Sustained ventricular tachycardia is associated with sudden cardiac death in HF.  About one-third of mortality in HF is due to sudden cardiac death.
  • 52. 52 Acute Decompensated HF  Cardiogenic pulmonary edema is a common and sometimes fatal cause of acute respiratory distress.  Characterized by the transudation of excess fluid into the lungs secondary to an increase in left atrial and subsequently pulmonary venous and pulmonary capillary pressures.
  • 53. 53 Acute Decompensated HF  Causes:  Acute MI o Rupture of chordae tendinae/acute mitral valve insufficiency  Volume Overload o Transfusions, IV fluids o Non-compliance with diuretics, diet (high salt intake)  Worsening valvular defect o Aortic stenosis
  • 54. 54 Acute Decompensated HF  Clinical manifestations:  Symptoms o Severe dyspnea o Cough
  • 55. 55 Acute Decompensated HF  Clinical manifestations:  Signs o Tachypnea o Tachycardia o Hypertension/Hypotension o Crackles on lung exam o Increased JVD(jagular venous distension) o S3, S4 or new murmur
  • 56. 56 Acute Decompensated HF  Investigations:  Chemistry, CBC  ECG  Chest X-ray  May consider cardiac enzymes  2D-Echo
  • 57. 57 Acute Decompensated HF  Treatment  Oxygen, mechanical ventilation if needed  Loop diuretics (Lasix)  Morphine  Vasodilator therapy (nitroglycerin)  Positive inotropes e.g Dobutmaine  Nesiritide (BNP) : can help in acute setting, for short term therapy
  • 59. 59 thanks F o r W a t c h i n g