undergraduates

2. HEART FAILURE
State in which the ventricles at normal filling pressures
cannot maintain an adequate cardiac output to meet the
metabolic needs of peripheral tissues.
It results from any structural or functional impairment of
ventricular filling or ejection of blood.

3. PATHOPHYSIOLOGY
Performance of heart depends upon for 3
essential components-
1.Contractility of muscle- force of contractions
generated by the myocardium under the given
loading conditions (↓)
2.Pre load- amount & pressure of blood in the
ventricle at the end of a diastole (↑)
3.After load- amount & pressure of blood in
ventricles during systole (↑)

4. COMPENSATORY
MECHANISMS
They are initially beneficial but later becomes
counterproductive, hence the manifestations.
1. ↑ myocardial contractility- ventricles dilate →vent.
Contractility ↑ → ↑ volume of blood ejected. But they can
be stretched to a limit beyond that it diminishes.
↑ LV Filling pressures are transmitted to pulmonary veins
→ alveolar transudation of fluid & pulmonary congestion →
O2 demand enhanced
2. Volume & pressure overload in vent. → myocardial
hypertrophy → ↑ CO → O2 demand ↑ → ↓ compliance of
ventricle → ↑ preload → transmitted to pul. Vasculature

5. COMPENSATORY
MECHANISMS
3. Sympathetic stimulation →
peripheral vasoconstriction →salt &
water retention
it also produces ↑ HR and enhances
contractility
4. Myocardial Remodelling

7. RISK FACTORS
Hypertension
Diabetes mellitus
Use of cardiotoxic substances ( alcohol, tobacco,
cocaine)
Hyperlipidemia
Thyroid disorders
Persistent Tachycardia
Coronary artery disease

8. CAUSES
Pressure
overload of
ventricle
1. Systemic
hypertenson
2. Pulmonary
hypertension
3.Aortic stenosis
4. Pulmonary
stenosis
Volume overload
of ventricle
1. Conditions
associated with ↑
metabolic demand
2. MR
3. AR
4. Ventricular
septal defect
5. PDA
6. Atrial septal
defect
Inflow
obstruction of
ventricle
1. Mitral stenosis
2. Tricuspid
stenosis
3.
Endomyocardial
fibrosis
Impaired
ventricular
function
1. Diffuse
myocardial dis-
myocarditis,
cardiomyopathy
2. Segmental
myocardial dis
3. MI

9. AGGREVATING CAUSES
Infections
Anaemia, pregnancy, thyrotoxicosis
Cardiac arrhythmias
Supervening heart diseases
Systemic hypertension
Pulmonary embolism
Excess salt intake
Stress
Poor compliance with therapy
ẞ blocker, steroids, NSAIDs

10. CLASSIFICATION

11. CLASSIFICATION

13. TYPES
LEFT,
RIGHT,
BIVENTRIC
ULAR
ACUTE AND
CHRONIC
LOW AND
HIGH
OUPUT
SYSTOLIC
AND
DIASTOLIC
FORWARD
AND
BACKWARD

14. ACUTE AND CHRONIC HF
ACUTE- develops suddenly
sudden reduced CO lead to systemic hypotension
without peripheral edema
CHRONIC- develops gradually
systemic arterial pressure maintained, edema
accumulates

15. TYPES
LEFT,
RIGHT,
BIVENTRIC
ULAR
ACUTE AND
CHRONIC
LOW AND
HIGH
OUPUT
SYSTOLIC
AND
DIASTOLIC
FORWARD
AND
BACKWARD

16. LOW & HIGH OUTPUT
HF
LOW OUTPUT- low CO, heart fails to
generate adequate output
HIGH OUTPUT- heart fails to maintain
sufficient circulation despite increased CO

17. TYPES
LEFT,
RIGHT,
BIVENTRIC
ULAR
ACUTE AND
CHRONIC
LOW AND
HIGH
OUPUT
SYSTOLIC
AND
DIASTOLIC
FORWARD
AND
BACKWARD

18. RIGHT, LEFT,
BIVENTRICULAR HF
LEFT- excess fluid accumulates upstream behind the
failing left ventricle
reduction in LV output, increase in LA pressure
& inc in pul. Venous pressure
RIGHT- excess fluid accumulates upstream behind
the failing right ventricle
reduction in RV output, resulting in systemic
venous congestion
BIVENTRICULAR- failure of both left and right
ventricles

19. TYPES
LEFT,
RIGHT,
BIVENTRIC
ULAR
ACUTE AND
CHRONIC
LOW AND
HIGH
OUPUT
SYSTOLIC
AND
DIASTOLIC
FORWARD
AND
BACKWARD

20. FORWARD & BACKWARD
HFFORWARD- dec CO & inadequate perfusion of
organs leading to poor tissue perfusion
Poor renal perfusion activates RAAS producing
excessive absorption of sodium by renal tubules
BACKWARD- normal CO, marked salt and water
retention , pulmonary and venous congestion

21. TYPES
LEFT,
RIGHT,
BIVENTRIC
ULAR
ACUTE AND
CHRONIC
LOW AND
HIGH
OUPUT
SYSTOLIC
AND
DIASTOLIC
FORWARD
AND
BACKWARD

22. SYSTOLIC & DIASTOLIC
HFSYSTOLIC- abnormality of ventricular contraction
Ejection fraction below 40%
DIASTOLIC- impaired ventricular relaxation, inc
ventricular stiffness, resulting in reduced filling
Preserved ejection fraction

23. CLINICAL
FEATURES
 Dyspnoea
 Orthopnoea
 Paroxysmal nocturnal dyspnoea
 Cardiac asthma
 Acute pulmonary oedema
 Cheyne stokes respiration
 Nocturia
 Cerebral symptoms ( confusion ,
memory impairment , anxiety )

24. CLINICAL
FEATURES
 Non specific symptom ( fatigue ,
weakness , low grade fever , anorexia ,
nausea , abdominal pain , fullness from
congestion of liver )
 Cardiac oedema
 Cyanosis
 Pulse ( pulsus alternans , sinus
tachycardia )

25. CLINICAL
FEATURES
 Blood pressure
 diminished pulse pressure due to
reduced stroke volume
 diastolic blood pressure may be
slightly raised occasionally due to
generalised vasoconstriction
 hypotension is prominent in acute
heart failure

26. CLINICAL
FEATURES
 Accentuated s3 and s4 in cardiac failure
 Respiratory system ( inspiratory
crepitations over lung bases )
 Congestive hepatomegaly
 Pleural effusion , ascites , pericardial
effusion
 Kidney ( oliguria , urinary sodium is low ,
specific gravity is high and proteinuria )
 Prerenal azotaemia

27. CLINICAL
FEATURES
 Cardiac cachexia
 Haematological feature ( anaemia )

28.  Dyspnoea
 Orthopnoea
 PND
 Acute pulmonary
Oedema.
 Tachypnoea, pallor ,
 Sweating
 Pulsus alternans
 S3 and s4 gallop
LEFT SIDED HF

29. RIGHT SIDED HF
 Anorexia
 Nausea , vomiting
 Right hypochondral
Pain
 Peripheral oedema
 Cyanosis
 Raised jvp
 Enlarged tender
Liver
 Ascites
 Pleural effusion

30. INVESTIGATIO
NS CHEST RADIOGRAPHY
 cardiomegaly
 prominence of upper lobe veins
 KERLEY B lines ( engorged peripheral
Lymphatics seen in lower lobe )
 BAT wing ( increased bronchovascular
Markings )
 pleural effusion
 Phantom tumour ( fluid in horizontal or
oblique fissure of lungs )

32. Engorged peripheral lymphatics in
lower lobe

33. Electrocardiograph
y Presence of ventricular hypertrophy
 Atrial abnormality
 Arrhythmias
 Conduction abnormalities
 Previous MI
 Active ischaemia

34. Brain natriuretic peptide
 Serum level increases in CHF
 Highly sensitive test
 Differentiate from respiratory cause of
acute dyspnoea

35. Other tests
 Assessment of ejection fraction ,
valvular functions , chamber size and
shape by echocardiography .
 Assessment of ejection fraction by
radionuclide ventriculography
 Ambulatory holter monitoring if
arrhythmias are suspected
 Renal and liver function test
 Thyroid function test

36. Management

37. Functional class 1
 ACE inhibitors
 Beta blockers
Management of chronic heart failure

38. Functional class 2
 Mild restriction of activity
 Mild sodium restriction
 ACE inhibitors
 Beta blockers
 Diuretics ( for volume overload )
 Digoxin ( if symptom persist )
 Aldosterone antagonist ( spironolactone)

39. Functional class 3
 Moderate restriction of activity
 Moderate sodium restriction
 Diuretics
 Spironolactone
 ACE inhibitors
 Beta blockers
 Digoxin
 Direct vasodilators ( if ACE inhibitors
contraindicated )

40. Functional class 4
 Severe restriction of activity
 Severe sodium restriction
 Diuretics
 Spironolactone
 ACE inhibitor
 Digoxin
 IV dopamine/dobutamine and amrinone

41. COMPLICATIONS
 Renal failure
 Hypokalaemia
 Hyperkalaemia
 Hyponatraemia
 Impaired liver function
 Thromboembolism
 Atrial & Ventricular Arryhthymias