Approach to Heart failure - An abnormality of Cardiac structure

1. Approach to
Heart Failure

2. Heart Failure
Heart Failure, is a clinical syndrome in which an
abnormality of cardiac structure or function is
responsible for the inability of the heart to eject
or fill with blood at a rate commensurate with the
requirements of metabolizing tissues

3. General Etiologies Of Cardiac Failure
1. CORONARY VASCULAR -> ACUTE MI
2. VALVULAR -> AORTIC , MITRAL VALVE DISEASE
3. MYOCARDIAL -> ISCHEMIC CARDIOMYOPATHY
4. HYPERTENSION -> HYPERTENSIVE CRISIS
5. RHYTHM DISTURBANCES -> TACHYCARDIA , INDUCED HF
6. PERICARDIAL -> TAMPONADE , CONSTRICTION

4. Underlying cardiac disease
Conditions that Conditions that
depress ventricular function restrict filling
CAD RESTRICTIVE C.M.PATHY
HTN PERICARDIAL DISEASE
DCM
Valvular heart disease
Congenital heart disease

5. Precipitating causes
1. Increased salt intake
2. Non compliance with anti CHF medications
3. Acute myocardial infarction
4. Aggravation of Hypertension
5. Acute arrhythmias
6. Infections and or fever

6. 1. Pulmonary Embolism
2. Anemia
3. Thyrotoxicosis
4. Pregnancy
5. Rheumatic, Viral, and Other Forms of Myocarditis
6. Infective Endocarditis
7. Physical, Environmental, and Emotional Excesses

7. Pathogenesis
1. Myocardial cell loss  myocyte hypertrophy and
elongation.
2. An increase in ventricular volume (the Starling
effect) helps maintain cardiac output (CO), but at
the cost of increasing ventricular filling pressures.
3. The increase in diastolic stretch and pressure
produces further damage stretch-induced
myocyte death (apoptosis)

8. CARDIAC OUTPUT
SYMPATHETIC DISCHARGE
REMODELLING
INC.FORCE
RATE
PRELOAD
AFTERLOAD
DEC. RENAL BLD FLOW
RAA. ACTIVATION
CARDIAC OUTPUT
SYMPATHETIC DISCHARGE
DEC. RENAL BLD FLOW
INC.FORCE
RATE
PRELOAD
AFTERLOAD
RAA. ACTIVATION
CARDIAC OUTPUT
SYMPATHETIC DISCHARGE
DEC. RENAL BLD FLOW

9. Forms of Cardiac Failure
1. Systolic and diastolic failure
2. Low output and high output failure
3. Acute and chronic heart failure
4. Backward and forward failure
5. Left and right heart failure

10. Approach to the patient
1. RESPIRATORY AND OTHER SYMPTOMS
2. Due to inadequate perfusion of peripheral tissues
1. Fatigue
2. Dyspnoea
3. Due to elevated intracardiac filling pressures
1. Orthopnoea
2. PND
3. Peripheral edema

11. Symptoms of heart failure
1. Respiratory Distress
2. Breathlessness- cardinal manifestation of left ventricular
failure
3. May present with progressively increasing severity as
1. exertional dyspnea
2. orthopnea
3. paroxysmal nocturnal dyspnea
4. dyspnea at rest
5. acute pulmonary edema.

12. Symptoms.
• URINARY SYMPTOMS.
1. Nocturia may occur early in the course of heart failure.
2. Oliguria is a sign of late cardiac failure.
• CEREBRAL SYMPTOMS.
1. Confusion, impairment of memory, anxiety, headache,
insomnia, bad dreams or nightmares, and, rarely, psychosis
with disorientation, delirium, and hallucinations.

13. Symptoms of predominant
right-sided Heart Failure
1. Breathlessness is not very prominent because pulmonary
congestion is usually absent.
2. Congestive hepatomegaly - dull ache or heaviness in
epigastrium.
3. Other gastrointestinal symptoms, including anorexia, nausea,
bloating, a sense of fullness after meals, and constipation
due to congestion of the liver and gastrointestinal tract.
4. In severe, preterminal heart failure, inadequate bowel
perfusion can cause abdominal pain, distention, and bloody
stools.

14. Physical examination
1. JVP
2. S3
3. Pulmonary congestion (rales, dullness over
pleural effusion)
4. Peripheral edema
5. Hepatomegaly
6. Ascites

15. Laboratory Investigations
1. CBC, ESR
2. Urine routine
3. LFT
4. RFT
5. CXR
6. ECHO
7. Measurement of BNP

16. BRAIN NATRIURETIC PEPTIDE (BNP)
• Pre pro-BNP is formed in the ventricles with
myocyte stretch
• Broken down to N-terminal-pro-BNP (NT-pro-
BNP) and BNP.
• Highly accurate for identifying or excluding HF
with high sensitivity and specificity
• BNP - valuable in differentiating cardiac from
pulmonary causes of dyspnea

17. Framingham Criteria for Diagnosis of
Congestive Heart Failure
One major +two minor for diagnosis
1. Paroxysmal nocturnal dyspnea
2. Neck vein distention
3. Rales
4. Cardiomegaly
5. Acute pulmonary edema
6. S3 gallop
7. Increased venous pressure (>16 cmH2O)
8. Positive hepatojugular reflux
9. Weight loss ≥4.5 kg over 5 days' treatment
Major Criteria

18. 1. Extremity edema
2. Night cough
3. Dyspnea on exertion
4. Hepatomegaly
5. Pleural effusion
6. Vital capacity reduced by one-third from normal
7. Tachycardia (≥120 bpm)
Minor Criteria

19. NYHA GRADING
• Class 1 : no symptoms
• Class 2 : symptoms with ordinary activity
• Class 3 : less than ordinary activity
• Class 4 : even at rest

20. Staging of systolic HF
1. STAGE A- ASYMPTOMATIC/ MILD HF NYHA CLASS 1
/ 2
2. STAGE B- MILD /MODERATE HF ,NYHA CLASS 2 / 3
3. STAGE C- ADVANCED HF , CLASS 3 / 4
4. STAGE D- REFRACTORY HF ,CLASS 3 / 4
5. SUSTAINED DECOMPENSATION, FREQUENT
HOSPITALISATION

21. Conditions That MIMIC CHF
1. Pulmonary disease
1. Chronic bronchitis
2. Emphysema
3. Asthma
2. Other causes of peripheral edema
1. Liver disease
2. Varicose veins
3. Cyclic edema
4. Renal dysfunction

22. General measures
1. Prevent HF
2. Daily measurement of weight
3. Immunization with influenza and pneumococcal
vaccines
4. Education of the patient and family
5. Avoid Excessive alcohol, temperature extremes,
and tiring trips
6. Meals - small in quantity, frequent
7. Reduce sodium intake

23. Activity
1. Releive anxiety.
2. Physical and emotional rest
3. Anticoagulants, leg exercises, and elastic
stockings.
4. Absolute bed rest is rarely required
5. Regular isotonic exercise
6. Weight reduction in obese

24. • Administration of oxygen
• Sleep apnoea - nocturnal continuous positive
airway pressure
• Dialysis or ultrafiltration in patients with
severe HF and renal dysfunction
• Other mechanical methods - theraputic
thoracocentesis or paracentesis .
• CORRECTION OF PRECIPITATING FACTORS

25. Measures for symptom relief
CONTROL OF EXCESSIVE FLUID
Diet
Diuretics
Thiazide diuretics
Loop diuretics
Metalazone
Potassium sparing diuretics

26. Role of diuretics
1. Rapid relief of symptoms
2. Controls fluid retention
3. Appropriate use of diuretics is the key
element in the success of other drugs

27. DIURETICS
• THIAZIDE DIURETICS -useful alone or in combination with
other diuretics
• In chronic mild HF
• K+ depletion and metabolic alkalosis
• Suited only if GFR >50%of normal
• METALAZONE
• Site of action and potency similar to the thiazides
• Effective in the presence of moderate renal failure
• Both metolazone and thiazides potentiate intravenous
loop diuretics

28. FUROSEMIDE, BUMETANIDE, AND
TORSEMIDE
• Useful in all forms of HF, particularly in refractory HF
and pulmonary edema.
• Effective in patients with hypoalbuminemia,
hyponatremia, hypochloremia, and with reductions
in glomerular filtration rate
• The action may be potentiated by I.V. administration
and by the addition of other diuretics

29. POTASSIUM-SPARING DIURETICS
• Spironolactone acts by competitive inhibition
of aldosterone
• Amiloride and triamterene act directly on the
distal tubule/collecting duct.
• Most effective with loop and/or thiazide
diuretics.
• Lower dose of spironolactone (25 mg/d),
prolong life in patients with advanced HF

30. Prevention of deterioration of cardiac
function or drugs increasing survival
1. Angiotensin converting enzyme (ACE
inhibitors)
2. Angiotensin receptor blockers
3. Aldosterone blockers
4. Beta adrenoceptor blockers

31. Angiotensin-Converting Enzyme (ACE)
Inhibitors
1. Prevention and treatment of HF at almost all
stages
2. Slows remodeling .
3. Cardiac output rises
4. Pulmonary wedge pressure falls,
5. Afterload is reduced with no or only mild
reduction of arterial pressure.
6. Signs and symptoms of HF are relieved

32. 1. Enhance exercise performance
2. Reduce long-term mortality .
3. Major effect of ACE inhibitors is on inhibition
of local (tissue) renin-angiotensin systems.
4. ACE inhibitor should be maintained
indefinitely.

33. ACE Inhibitor in cardiac failure
Name Starting dose Target
Enalapril 1.25-2.5 BD 10 BD
Captopril 6.25-12.5 TID 25-50 TId
Lisinopril 2.5-5 0D 20-35 OD
Ramipril 1.25 -2.5 BD 5 BD

34. ARB
1. Equally effective
2. ACE inhibitor intolerance

35. BETA BLOCKERS
Drug Start Target
Carvedilol 3.125 bd 25bd
Bisoprolol 1.25 od 10 od
Metoprolol 12.5 -25 od 200bd
• As ADD on therapy with diuretics and ACEI
• Improves ejection fraction,exercise tolerance lowers
rate ,dec.myo O2 demand,,reduces arrythmias
reverse LVH,prevents sudden deaths

36. Use of Beta blockers
1. Optimise volume status
2. Start at lowest possible dose
3. Increase dose gradually
4. Monitor vital signs ,wt , clinical profile

37. Enhancement of Cardiac contractility
1. Digitalis,digoxin oubain
2. Sympatho mimetic amines
3. Phosphodiesterase inhibitors

38. When should Digoxin be used

39. DIGOXIN
1. Positive inotropic response
2. Inhibit Na+, K+-ATPase
3. Effective in systolic HF complicated by atrial flutter
and fibrillation and a rapid ventricular rate
4. Does not improve survival in patients with systolic
HF and sinus rhythm, it reduces symptoms of HF
5. No value in diastolic HF.

40. Sympathomimetic Amines
1. Dopamine and dobutamine ,dopexamine
2. Act on β-adrenergic receptors
3. Improve myocardial contractility
4. In severe, acute HF
5. Constant intravenous infusion
6. Can be given for several days
7. Used in refractory HF as a “bridge” to cardiac
transplantation.
8. “Downregulation” of adrenergic receptors

41. Phosphodiesterase Inhibitors
1. Amrinone,milrinone,enoximone,piroximone,fen
oximone
2. Inhibit phosphodiesterase III
3. Positive inotropic and vasodilator actions
4. Administered intravenously
5. Reverse the major hemodynamic
abnormalities associated with HF

42. Vasodilators
1. Useful in severe, acute HF with significant systemic
vasoconstriction despite ACE inhibitor therapy.
2. Rapid onset and brief duration of action
3. Sodium nitroprusside
4. Intravenous nitroglycerin 20micg/min max
400micg/min
5. Nesiritide iv bolus 2micg/kg+0.01micg/kg/min
6. Combination of hydralazine and isosorbide dinitrate
- for chronic oral administration

43. Nesiritide, a recombinant analog of BNP
1. The newest therapeutic option for ADHF.
2. Increase natriuresis, diuresis, and cardiac index
3. Reduce pulmonary capillary wedge pressure,
pulmonary artery pressure, pulmonary vascular
resistance, and systemic blood pressure in a dose-
dependent manner.
4. Reversal of the deleterious neurohormonal response
associated,with HF
5. Reduces levels of endothelin 1, aldosterone,and
norepinephrine.

44. • Nesiritide is more effective than nitroglycerin
in producing rapid and significant reduction of
LV filling pressures
• Does not require ICU admission or invasive
monitoring .
• Lower incidence of tachycardia and
proarrhythmic effects.
• Lessen the need for supportive therapies such
as diuretics

45. Survival benefit of different drugs
• Those which reduce MORTALITY
• Those which Increase MORTALITY
• Those without any proved influence on
MORTALITY

46. Reduce mortality
1. Beta Blockers
2. A.C.E. Inhibitors
3. Angiotensin Receptor Blockers
4. Spironolactone
5. Amiodarone

47. Drugs increasing Mortality
1. Inotropes&Inotropic dilators
2. Antiarrythmics except
1. betablockers&Amiodarone
3. Calcium Channelblockers
4. High dose Digoxin

48. Diuretics
Digoxin(low dose)
Nitrate
Those without any proved
influence on MORTALITY

49. Fluid retention +
Assess volume status
Beta blockers
ACE 1
Diuretic titrate to euvolemic
No fluid retention
LVEF <40 %

50. VENTRICULAR RESYNCHRONIZATION
1. Intraventricular conduction is depressed in about
one-fourth of patients with chronic HF
2. “Resynchronization” with a device that has three
pacing leads (right atrium, right ventricle, and
cardiac vein, which provides left ventricular
stimulation) improve performance in patients with
HF
3. Increase ejection fraction

51. MANAGEMENT OF ARRHYTHMIAS
1. Premature ventricular contractions and
episodes of asymptomatic ventricular
tachycardia are common in advanced HF
2. VT/VF is responsible for about one-half of all
deaths
3. Correction of electrolyte and acid-base
disturbances

52. Amiodarone
1. Amiodarone, a class III
antiarrhythmicis the drug of choice
for patients with HF and atrial
fibrillation.
2. Implantable automatic defibrillator
prevent sudden deaths

53. Anticoagulants
1. Increased risk of pulmonary emboli secondary to
venous thrombosis and of systemic emboli
secondary to intracardiac thrombi
2. Patients with HF and atrial fibrillation, previous
venous thrombosis, and pulmonary or systemic
emboli are at high risk
3. Heparin followed by warfarin

54. Management of Diastolic HF
1. HTN regression of LVH important ……ARB,ACE
2. Myocardial ischemia…….. Bblockers ,CCB,nitrates
3. Chronic AF……. restore sinus rythmn,rate control
4. Beta blocker…… slow rate ,reduce O2 demand,lower
BP,regress LVH
5. CCB has lusiotropic effect (relaxation enhancing effect)
6. ACE inh. Effect uncertain ……ARB use regress LVH
7. Exercise conditioning….. improves diastolic function
,dynamic isotonic exercise ideal
8. Better Prognosis
9. Bad prognosis-Older age ,males ,lower
ej.fraction,ass,CAD,DM,impaired renal function

55. Management Of ADHF
• Administration of oxygen
• Morphine sulfate
• Mechanical ventilation is indicated
• A sitting position improves pulmonary
function.
• Placing the patient on strict bed rest and
reducing pain and anxiety decrease cardiac
workload.

56. 1. Intravenous inotropes and vasodilators - The
combination of an intravenously administered
vasodilator such as nitroglycerin, niseritide, or of a
phosphodiesterase inhibitor together with a
sympathomimetic amine
2. Hemodynamic monitoring cvc,swan ganz
catheter,O2 saturation
3. Extracorporeal ultrafiltration and hemofiltration-
Acute hemodialysis and ultrafiltration may be
effective, especially in the patient with significant
renal dysfunction and diuretic resistance ,removes
i.v fluid

57. 1. Mechanical circulatory supports
2. Devices
1. Counter pulsation device(Intra aortic baloon
pump and non invasive counter pulsation)
2. Cardiopulmonary assist devices
3. Left ventricular assist devices

58. • In hospitalized patients with refractory HF, therapy to
be guided by hemodynamic measurements by a
balloon flotation (Swan-Ganz) catheter
• The goal is to achieve pulmonary capillary wedge
pressure of 15 to 18 mmHg
• Right atrial pressure of 5 to 8 mmHg
• Cardiac index >2.2 L/min per m2
• Systemic vascular resistance of 800 to 1200 dyne ·
s/cm5.

59. SURGICAL THERAPY
• CARDIAC TRANSPLANTATION best predictor peak O2
consumption with maximal exercise (VO2max)NI
>20ml/kg/min,<10ml/kg/min ……transplantation
ideal
• Novel surgeries
– Ventricular remodelling surgeries
– Dynamic cardiomyoplasty
– Mitral valve repair

60. NEWER Rx MODALITIES FOR ADHF
1. BALOON COUNTER PULSATION –
INTRAAORTIC BALOON PUMP
2. VAD – PULSATILE LOW FLOW VAD
3. PACING – BIVENTRICULAR PACING , AV
SEQUENTIAL PACING

61. B N P analogue
Nesiritide
Endopeptidase inhibitor(ACE+neutral peptidases)
Omapatrilat
NEWER DRUGS

62. Pimobendan,Levosibendan
• LEVOSIBENDAN is a novel agent with inotropic
properties developed specifically for the
management of ADHF.
• It acts by sensitizing troponin C to calcium
Calcium Sensitiser

63. Endothelin receptor antagonist
BOSENTAN
TEZOZENTAN
Effective in acute coronary syndromes, acute
renal failure and acute HF.
• Indirectly improve contractility while
decreasing pulmonary capillary wedge
pressure.

64. • VASOPRESSIN ANTAGONISTS (V2 RA)
Tolvaptan, Lixiraptan ,Coniraptan
– CAN BE USED AS ADJUVANT to DIURETIC IN ADVANCED HF
• ENOXIMONE –TYPE 3 PDEI
– PA Pr. MONITORING REQUIRED
– LV FILLING PRESSURE > 15 mm Hg
– IDEAL INOTROPE FOR PATIENT ON
ß BLOCKERS

65. PROGNOSIS
1. Depends primarily on the nature of the underlying
heart disease
2. Presence or absence of a precipitating factor
3. Prognosis can be estimated by observing the
response to treatment.
4. When patients can be rendered free of congestion,
survival may be 80% at two years.

66. 1. High BUN (>43 mg/dL) is the best single
predictor of inhospital mortality
2. Severely depressed ejection fraction<15%
3. Inability to walk on level at normal
pace>3min
4. Low SBP (<115 mm Hg)
5. High serum creatinine (SCr) levels (>2.75
mg/dL).
6. Elevations in circulating levels of B-type
natriuretic peptide (BNP)
7. Cardiac necrosis marker troponin I

67. When all available therapeutic
measures have been exhausted,
comfort care, with continued
infusions of inotropic agents,
diuretics, and the administration
of anxiolytics and analgesics
should be considered.