pathophysiologic state in which an abnormality of cardiac function is responsible for the failure of the heart to pump blood at a rate commensurate with the requirements of the metabolizing tissues or can do so only from an abnormally elevated diastolic volume

1. S. L. Pitmang
Department of Family Medicine
Jos University Teaching Hospital.

2.  Heart failure
 pathophysiologic state
 in which an abnormality of cardiac function is
responsible for the
 failure of the heart to pump blood at a rate
commensurate with the requirements of the
metabolizing tissues
 or
 can do so only from an abnormally elevated
diastolic volume
2

3.  The CO is the function of PL(vol. and
pressure of blood in the ventricle at the end
of diastole), the AL(the arterial resistance)
and the myocardial contractility.
 In the absence of valvular lesion the primary
abnormality in HF is impairment of
ventricular function leading to fall in CO.
 This activates counter-regulatory
neurohormonal mechanisms which in normal
physiological circumstances would support
function, but in the setting of impaired
ventricular function can lead to a deleterious
increase in both AL &PL
3

4.  A vicious cycle may be established bcos any
additional fall in CO will cause further
neurohormonal activation and increase in
peripheral vascular resistance.
 Stimulation of RAAS leads to
vasoconstriction, salt and H20 retention and
sympathetic activation mediated by
angiotensin II, being a potent
vasoconstrictor of efferent arterioles in the
kidney and systemic circulation.
 Activation of the SS may initially maintain
CO through an increase in MC, HR and
peripheral vasocontriction.
4

5.  However prolonged sympathetic stimulation
leads to cardiac myocyte apoptosis(cell
death), hypertrophy and focal myocardial
necrosis.
 Salt and H20 retention is promoted by release
of aldosterone, endothelin(a potent
vasoconstrictor peptide with marked effects
on the renal vasculature) and, in severe HF,
ADH.
 N-peptides are released from the atria, in
response to atrial stretch acting as
physiological antagonist to fluid conserving
effect of aldosterone, however they are
shortlived.
5

6.  After MI, CC is impaired and
neurohormonal activation may lead to
hypertrophy of non-infarcted segments
with thinning, dilatation and expansion of
the infarcted segment(remodelling). This
leads to further deterioration in
ventricular function and worsening HF.
 The onset of pulmonary and/ or
peripheral oedema is due to high atrial
pressure compounded by salt & H20
retention caused by impaired renal
perfusion and secondary aldosteronism.
6

7.  HF reflects the impairment of the left or
right ventricle.
 Left ventricular (LV) failure
 coronary artery disease,
 hypertension,
 most forms of cardiomyopathy
 congenital defects (e.g. ventricular septal
defect, patent ductus arteriosus with large
shunts).
7

8.  Right ventricular (RV) failure
 commonly caused by prior LV failure (which
increases pulmonary venous pressure and leads
to pulmonary arterial hypertension)
 tricuspid regurgitation
 Mitral stenosis
 primary pulmonary hypertension
 multiple pulmonary emboli
 pulmonary artery or valve stenosis
 RV infarction are also causes
8

9.  Volume overload and increased systemic venous
pressure
 simulating HF
 myocardial function may be normal.
 occur
 polycythaemia
 overtransfusion
 acute renal failure with overhydration
 obstruction of either vena cava.
9

10.  systolic dysfunction
 (primarily a problem of ventricular contractile
dysfunction),
 the heart fails to provide tissues with adequate
circulatory output.
 numerous causes;
 the most common are
 coronary artery disease,
 hypertension
 dilated congestive cardiomyopathy.
10

11.  Diastolic dysfunction
 resistance to ventricular filling
 not readily measurable at the bedside
 accounts for 20 to 40% of cases of HF.
 generally associated with prolonged ventricular
relaxation time,
 causes
 hypertrophic cardiomyopathy,
 ventricular hypertrophy (e.g. hypertension, advanced
aortic stenosis)
 amyloid infiltration of the myocardium.
11

12.  High output failure
 associated with a persistent high CO that
eventually results in ventricular dysfunction.
causes
 anaemia
 beriberi
 thyrotoxicosis
 pregnancy
 advanced Paget's disease
 arteriovenous fistula.
 CHF may develop in high-output states
 reversible by treating the underlying cause.
12

13.  HF may be predominantly right-sided or left-
sided
 may develop gradually
 or suddenly (acute pulmonary oedema).
13

14.  Cyanosis
 may occur with any form of HF
 may be central and may reflect hypoxemia.
 peripheral component due to capillary stasis
with increased A-VO2 and resultant marked
venous oxyhaemoglobin unsaturation may also
be present.
 Improved colour of the nail bed with vigorous
massage suggests peripheral cyanosis.
 Central cyanosis cannot be altered by
increasing local blood flow.
14

15.  Signs of chronic LV failure
 diffuse and laterally displaced apical impulse
 palpable and audible ventricular (S3) and atrial
gallops (S4),
 accentuated pulmonic second sound,
 and inspiratory basilar rales.
 Right-sided pleural effusion is common.
15

16.  Pulmonary venous hypertension
 may become apparent with tachycardia,
 fatigue on exertion,
 dyspnoea on mild exercise
 and intolerance to cold.
 Paroxysmal nocturnal dyspnoea and
nocturnal cough reflect the redistribution
of excess fluid into the lung with the
recumbent position.
16

17.  Occasionally, pulmonary venous hypertension and
increased pulmonary fluid manifest as
bronchospasm and wheezing.
 Cough may be prominent, and pink-tinged or
brownish sputum due to blood
 Frank haemoptysis due to ruptured pulmonary
varices with massive blood loss is uncommon but
may occur.
17

18.  a life-threatening manifestation of acute LV
failure
 secondary to sudden onset of pulmonary
venous hypertension.
 A sudden rise in LV filling pressure
 results in rapid movement of plasma fluid
through pulmonary capillaries into the interstitial
spaces and alveoli.
18

19.  extreme dyspnoea,
 deep cyanosis,
 tachypnoea,
 hyperpnoea,
 restlessness,
 and anxiety with a sense of
suffocation.
 Pallor and diaphoresis are
common.
 The pulse may be thready,
 BP may be difficult to
obtain.
 Respirations are
laboured,
 Crepitations are widely
dispersed over both
lung fields anteriorly
and posteriorly.
 Some patients manifest
marked bronchospasm
or wheezing (cardiac
asthma).
 summation gallop,
merger of S3 and S4,
may be heard
19
The patient presents with

20.  principal symptoms include
 fatigue;
 awareness of fullness in the neck;
 fullness in the abdomen,
 right upper quadrant abdominal pain (over the
liver);
 ankle swelling
 in advanced stages
 abdominal swelling due to ascites.
 Oedema over the sacrum in supine patients.
20

21.  Signs include evidence of systemic venous
hypertension
 abnormally large a or v waves in the external
jugular pulse,
 an enlarged and tender liver
 murmur of tricuspid regurgitation along the
left sternal border,
 RV S3 and S4
 pitting oedema of the lowest parts of the body.
21

22.  The European Society of Cardiology's
guidelines require there to be both symptoms
of heart failure (for example, breathlessness,
fatigue, ankle swelling) and objective
evidence of cardiac dysfunction (systolic or
diastolic, at rest) before the diagnosis is
made.
 Heart failure may have a number of different
aetiologies (as outline above) – always try
and determine the cause. Left ventricular
failure (LVF) and right ventricular failure
(RVF) may occur independently, or together
as congestive cardiac failure (CCF).
22

23. Heart failure should never be the
only diagnosis, as it is a syndrome
occurring as a result of other
diagnostic entities.
Diagnosis of HF cannot be made
until the heart is found to be
abnormal, and there is pulmonary or
systemic venous congestion
23

24. symptoms and signs are fairly
obvious
 (e.g., exertional dyspnoea,
orthopnoea, oedema, tachycardia,
pulmonary rales, a third heart
sound, jugular venous distension)
diagnostic specificity of 70 to 90%,
the sensitivity and predictive
accuracy are low.
24

25.  Physical signs of an abnormal heart are
usually obvious except in cardiac
constriction( EMF), cardiac
compression(acute pericardial effusion)
and rarely in patients with severe mitral
stenosis.
 In patients with systemic venous
congestion, the triad of oedema ascites
and large tender liver may mimic liver
disease. Look for abnormal heart, and
high venous pressure.
25

26.  Other possible causes of oedema are:
-Hypoalbuminaemia: look also for silken hair and patch
depigmentation
-Nephrotic syndrome: look for heavy proteinuria: the heart
is normal.
 The congested liver may be mistaken for
liver abscess, unless the jugular veins are
carefully examined.
 Children with HF may be thought to have
liver disease as the tender liver obscures
other signs; the tachycardia of acute
rheumatic carditis may be thought to due to
infection
26

27.  Fever and tachypnoea in a previously well
person are often due to acute pneumonia:
signs of consolidation are not found within
the first few days.
 PCP in pts with immunosuppression due to
HIV infection, Pulmonary KS, diffuse PTB may
give physical signs like pulmonary
congestion, so look for other HIV/AIDS
related signs.
 Breathlessness and wheezing, due to
bronchial asthma may be a difficult problem.
27

28.  Cor pulmonale associated with COAD with
respiratory failure may present in HF: A long
standing hx of respiratory symptoms with
signs of airway obstruction with thoracic
distortion, are helpful.
 Acute lobar pneumonia sometimes presents
as pulmonary oedema
 Other causes of pulmonary oedema include
head injury or CVA, acute viral encephalitis,
malaria and uraemia.
28

29.  FBC, U&E and creatinine, LFT's, glucose,
fasting lipids, thyroid function tests; consider
cardiac enzymes if an MI is possible in the
last few days.
 12-lead-ECG: This may elucidate the cause of
heart failure (e.g. SVT/AF, Q-waves
suggesting previous MI; also look for
ischaemic ST changes, bundle branch block,
atrial fibrillation, left axis deviation, and
ventricular hypertrophy). A normal ECG
makes LVSD unlikely (negative predictive
value of 98%).11
29

30.  Echocardiography is the key test to provide a
semi-objective assessment of cardiac
function.
 It is increasingly available "open access" to
F/P and should be performed in almost all
patients with symptoms or signs of heart
failure. Those with murmurs, atrial
fibrillation, at "high risk" for LVSD (post MI,
arrhythmias or poorly controlled
hypertension), or where the diagnosis/cause
of heart failure is uncertain, are prime
candidates for echocardiography
30

31.  CXR: Cardiomegaly (cardiothoracic ratio
>50%), prominent upper lobe veins (upper
lobe diversion), peribronchial cuffing, diffuse
interstitial or alveolar shadowing, fluid in the
fissures, pleural effusions, Kerley B lines. The
pulmonary shadowing may be classical
perihilar "bat's wings" or occasionally
unilateral (if nursed on one side), or nodular
(especially with pre-existing COPD).
31

32. 32

33. 33

34.  Additional Tests:
 Consider 24 hr ECG to detect paroxysmal
arrhythmias.
 Measurement of N-Terminal pro-brain
natriuretic peptide (NT-pro-BNP) has been
shown to be consistently elevated in heart
failure. It is a good predictor of death and
cardiovascular events in acute and chronic
heart failure patients. It has been
demonstrated that its use improves diagnostic
accuracy in a community setting. It is also very
useful as a guide to optimisation of therapy.
34

35.  B-Type (or brain) natriuretic peptide (BNP) is
useful to exclude LVF as cause of dyspnoea – if
a patient presents with breathlessness and has
a low BNP, a cardiac cause is unlikely. The use
of BNP tests to rule out heart failure in primary
care has the potential to reduce demand for
echocardiography.
 Radionuclide imaging may be helpful to assess
global ventricular function when
echocardiography is not possible.
 Endomyocardial biopsy is rarely needed.
35

36.  This may be assessed using a standardised
exercise test or the six minute walk test
(which strongly and independently predicts
morbidity and mortality in patients with left
ventricular dysfunction).Remember most
patients do not show a linear deterioration,
but may fluctuate even in the absence of
treatment changes, and changes in
treatment may make things better, or worse,
in the absence of measurable changes in
ventricular function.
36

37.  Class I: No symptoms on ordinary physical
activity
 Class II: Slight limitation of physical activity
by symptoms
 Class III: Less than ordinary activity leads to
symptoms
 Class IV: Inability to carry out any activity
without symptoms
37

38.  Stage A: Patients at high risk for developing
HF in the future but no functional or
structural heart disorder;
 Stage B: a structural heart disorder but no
symptoms at any stage;
 Stage C: previous or current symptoms of
heart failure in the context of an underlying
structural heart problem, but managed with
medical treatment;
 Stage D: advanced disease requiring hospital-
based support, a heart transplant or
palliative care.
38

39.  Diet and life style measures
 Pharmacological treatment
39

40. Patients with CHF are educated to undertake
various non-pharmacological measures to
improve symptoms and prognosis. Such
measures include;
 Moderate physical activity, when symptoms
are mild or moderate; or bed rest when
symptoms are severe.
 If sleep apnea is identified, treat with CPAP,
dental appliances or surgery. Sleep apnea is
an under recognized risk factor for heart
failure
40

41.  Weight reduction – through physical activity
and dietary modification, as obesity is a risk
factor for heart failure and left ventricular
hypertrophy.
 Monitor weight - this is a parameter that can
easily be measured at home. Rapid weight
increase is generally due to fluid retention.
Weight gain of more than 2 kilograms is
associated with admission to the hospital for
heart failure
 Sodium restriction – excessive sodium intake
may precipitate or exacerbate heart failure,
thus a "no added salt" diet (60–100 mmol
total daily intake) is recommended for
patients with CHF. More severe restrictions
may be required in severe CHF 41

42.  Fluid restriction – patients with CHF have a
diminished ability to excrete free water
load.
 Hyponatremia frequently develops in
decompensated heart failure due to the
effects of excess circulating neuroendocrine
hormones.
 While the activation of the renin-
angiotensin-aldosterone axis due to
decreased renal perfusion promotes both
sodium and water retention.
 Generally water intake should be limited to
1.5 L daily or less in patients with
hyponatremia.
42

43.  Systemic oedema and even pulmonary
oedema can be treated in the outpatient
clinic; when beds are few, admission is
necessary if the patient has:
-Travelled far and has nowhere to stay
-Severe symptoms of breathlessness and cough
-Any complication of cardiac failure
-A disease which demands hospital care, e.g. Infective
endocarditis
43

44. Treatment is designed to:
 Reduce the expanded ECF volume(blood and
interstitial fluid volumes) and induce a sodium
diuresis- by diuretics
 Reduce the work of the heart, by after-load and
pre-load reduction, by ACE inhibitors and
vasodilators
 Increase the tone of cardiac muscle- by digoxin
 Correct neurohumoral disturbances with ACE
inhibitors and beta-blockers.
 Correct the underlying cause of cardiac failure,
if possible eliminate any associated diseases.
44

45. • Diuretics
• ACE inhibitors
• Beta Blockers
• Digitalis
• Spironolactone
• Other
45

46.  Diuretics. Indications
 1. Symptomatic HF, with fluid
retention
• Edema
• Dyspnea
• Lung Rales
• Jugular distension
• Hepatomegaly
• Pulmonary edema (Xray)
46

47. Loop Diuretics / Thiazides. Practical Use
•Start with variable dose. Titrate to
achieve dry weight
•Monitor serum K+ at “frequent
intervals”
•Reduce dose when fluid retention is
controlled
•Teach the patient when, how to change
dose
•Combine to overcome “resistance”
•Do not use alone

48. Thiazides, Loop Diuretics. Adverse Effects
• K+, Mg+ (15 - 60%) (sudden death ???)
• Na+
• Stimulation of neurohormonal activity
• Hyperuricemia (15 - 40%)
• Hypotension. Ototoxicity. Gastrointestinal.
Alkalosis. Metabolic
Sharpe N. Heart failure. Martin Dunitz 2000;43
Kubo SH , et al. Am J Cardiol 1987;60:1322
MRFIT, JAMA 1982;248:1465
Pool Wilson. Heart failure. Churchill Livinston 1997;635

49. Diuretic Resistance
• Neurohormonal activation
• Rebound Na+ uptake after volume loss
• Hypertrophy of distal nephron
• Reduced tubular secretion (renal failure, NSAIDs)
• Decreased renal perfusion (low output)
• Altered absortion of diuretic
• Noncompliance with drugs
Brater NEJM 1998;339:387
Kramer et al. Am J Med 1999;106:90

50. Managing Resistance to Diuretics
• Restrict Na+/H2O intake (Monitor Natremia)
• Increase dose (individual dose, frequency, i.v.)
• Combine: furosemide + thiazide / spiro / metolazone
• Dopamine (increase cardiac output)
• Reduce dose of ACE-i
• Ultrafiltration
Motwani et al Circulation 1992;86:439

51. ACE-I. Clinical Effects
• Improve symptoms
• Reduce remodelling / progression
• Reduce hospitalization
• Improve survival

52. • Symptomatic heart failure
• Asymptomatic ventricular dysfunction
- LVEF < 35 - 40 %
• Selected high risk subgroups
ACE-i. Indications
AHA / ACC HF guidelines 2001
ESC HF guidelines 2001

53. ACE-i. Practical Use
•Start with very low dose
•Increase dose if well tolerated
•Renal function & serum K+ after 1-2 w
•Avoid fluid retention / hypovolemia (diuretic use)
•Dose NOT determined by symptoms
•Combine to overcome “resistance”
•Do not use alone

54. ACE-I. Adverse Effects
• Hypotension (1st dose effect)
• Worsening renal function
• Hyperkalemia
• Cough
• Angioedema
• Rash, ageusia, neutropenia, …

55. ACE-I. Contraindications
• Intolerance (angioedema, anuric renal fail.)
• Bilateral renal artery stenosis
• Pregnancy
• Renal insufficiency (creatinine > 3 mg/dl)
• Hyperkalemia (> 5,5 mmol/l)
• Severe hypotension

56. ß-Adrenergic Blockers
Mechanism of action
• Density of ß1 receptors
•Inhibit cardiotoxicity of catecholamines
• Neurohormonal activation
• HR
•Antiischemic
•Antihypertensive
•Antiarrhythmic
•Antioxidant, Antiproliferative

57. ß-Adrenergic Blockers
Clinical Effects
• Improve symptoms (only long term)
• Reduce remodelling / progression
• Reduce hospitalization
• Reduce sudden death
• Improve survival

58. • Symptomatic heart failure
• Asymptomatic ventricular dysfunction
- LVEF < 35 - 40 %
• After AMI
AHA / ACC HF guidelines 2001
ESC HF guidelines 2001
ß-Adrenergic Blockers
Indications

59. •Patient stable
• No physical evidence of fluid retention
• No need for i.v. inotropic drugs
•Start ACE-I / diuretic first
•No contraindications
•In hospital or not
ß-Adrenergic Blockers
When to start

60. Digitalis. Mechanism of Action
Blocks Na+ / K+ ATPase => Ca+ +
• Inotropic effect
• Natriuresis
• Neurohormonal control
- Plasma Noradrenaline
- Peripheral nervous system activity
- RAAS activity
- Vagal tone
- Normalizes arterial baroreceptors
NEJM 1988;318:358

61. Digitalis. Clinical Effects
• Improve symptoms
• Modest reduction in hospitalization
• Does not improve survival

62. Digitalis. Indications
• When no adequate response to
ACE-i + diuretics + beta-blockers
AHA / ACC Guidelines 2001
• In combination with ACE-i + diuretics
if persisting symptoms
ESC Guidelines 2001
• AF, to slow AV conduction
Dose 0.125 to 0.250 mg / day

63. • Digoxin toxicity
• Advanced A-V block without pacemaker
• Bradycardia or sick sinus without PM
• PVC’s and VT
• Marked hypokalemia
• W-P-W with atrial fibrillation
Digoxin. Contraindications

64. Spironolactone. Indications
• Recent or current symptoms despite
ACE-i, diuretics, dig. and b-blockers
AHA / ACC HF guidelines 2001
• Recommended in advanced heart failure
(III-IV), in addition to ACE-i and diuretics
• Hypokalemia
ESC HF guidelines 2001

65. Spironolactone. Practical use
• Do not use if hyperkalemia, renal insuf.
• Monitor serum K+ at “frequent intervals”
• Start ACE-i first
• Start with 25 mg / 24h
• If K+ >5.5 mmol/L, reduce to 25 mg / 48h
• If K+ is low or stable consider 50 mg / day
New studies in progress

66. Other Drugs. (only in selected patients)
• Inotropics: refractory HF
• Nitrates: ischemia, angina, pulmonary congestion
• ARB: Contraindications to ACE-i
• Antiarrhythmics: (only amiodarone) H risk arrhyth.
• Anticoagulants: High risk of embolysm
• Ca channel blockers: (only amlodipine) ischemia

67.  Although the outlook depends to some extent
on the underlying cause of the problem, HF
carries a very poor prognosis.
 Approximately 50% of patients with severe HF
due to left ventricular dysfunction will die
within 2 years.
 Many patients die suddenly from malignant
ventricular arrhythmias or myocardial
infarction.
67

68. 68