We a group of students from Najran University made a seminar about heart failure talks about various aspect of the topic.

1. Heart
Failure
Group: B

2. Objectives:
– 1-physiology of cardiac output
– 2-Definition , Epidemiology and Etiology.
– 3-Pathophysiology of the heart failure.
– 4-Types of heart failure.
– 5-Classifications of the heart failure
– 6-Clinical features of heart failure
– 7-Investigations of heart failure
– 8-Treatment and prevention of heart failure
– 9-Complications of heart failure.

3. physiology of heart
(cardiac output)
MOHAMMED AHMED ALQADI

4. CARDIAC OUTPUT
* Definitions:
Cardiac output:
Cardiac output )COP( is the volume of blood (liters) pumped by each ventricle per
minute.
Cardiac output (COP) = stroke volume (SV) x heart rate (HR)

5. CARDIAC OUTPUT
Heart rate(HR):
Heart rate is the number of heart beats per minute. It is
about 70 beat/minute.
Stroke volume:
Stroke volume (SV) is the volume of blood pumped by each
ventricle per beat. It is about 70 ml/beat.

6. CARDIAC OUTPUT
End diastolic volume:
End diastolic volume (EDV) is the volume of blood in the
ventricle at the end of diastole. It is about 135 -140 ml.
End systolic volume:
End systolic volume (ESV) is the volume of blood in the ventricle
at the end of systole. It is about 70 ml (from 65 -70 ml).

7. CARDIAC OUTPUT
.
Ejection fraction:
-It is the percentage of the SV to the end diastolic volume.
-It ranges between 50-65%.
It increases in increased contractility and decreases in
increased aortic resistance and in heart failure

8. CARDIAC OUTPUT
B-Cardiac output is increased in:
1- Excitement: increase COP by about 50 -100% due to sympathetic
stimulation.
2- Exposure to extremes of temperature:
● In high temperature due to skin vasodilatation.
3- Eating: in the first few hours after eating due to increase GIT blood flow.
4- Exercise: exercise can increase COP up to 700% in trained athletes
5- Pregnancy: due to increase uterine blood flow and placental arterio-
venous shunt. The blood volume in pregnant increases about 40%.

9. C- Cardiac output is decreased in:
1- Sitting or standing from lying down decrease COP by 20 -30%.
However under normal condition immediate compensation occurs by
constriction of veins→ increase venous return→ increase COP.
2- Marked arrhythmia (tachycardia or bradycardia).
●In tachycardia: COP is decreased due to shortening of the diastolic
period in which cardiac filling occur.
●In bradycardia: although the SV is increased it cannot compensate for
the decreased HR.
3-In all conditions which destroy the cardiac muscle fibers.

10. CARDIAC OUTPUT
REGULATION OF CARDIAC OUTPUT
I-Contractility:
Increase the force of cardiac muscle contractility depends on two
independent mechanisms (intrinsic and extrinsic)
1- Intrinsic regulation:
-This mechanism affects only the SV by affecting contractility and
include heterometric and homeometric autoregulation

11. CARDIAC OUTPUT
(a) Heterometric autoregulation (Starling law):
It is the ability of the cardiac muscle to increase its force of contraction
secondary to increase in the EDV (preload). Increased contraction leads
to increase in SV and COP.
b) Homeometric autoregulation.
This mechanism occurs in prolonged exercise.
The mechanism of increased contractility in homeometric autoregulation is
the increase in intra-ventricular pressure and aortic pressure (after load)
produced during heterometric autorgulation. Also, increase in coronary
blood flow and increase intracellular Ca++ .

12. CARDIAC OUTPUT
2-Extrinsic regulation:
A- Autonomic nervous system:
●Sympathetic nervous system increases COP due to:
1- Increase HR (positive chronotropic effect )
2- Increased contractility (positive inotropic effect)
3- Venoconstriction which increases venous return and filling of
the heart.
●Parasympathetic N.S. decreases COP through decreasing HR

13. CARDIAC OUTPUT
B- Chemical Factors:
- Chemicals that increase C.O.P Hypereffective heart:
 Catecholamines →↑cAMP →↑Ca++influx.
 Digitalis (Digoxine) increases C.O.P in heart failure by increase of
intracellular Ca++ and force of contraction
 Glucagon (Pancreatic hormone) activate adenyl cyclase enzyme
→↑cAMP →↑Ca++influx

14. CARDIAC OUTPUT
IV. Venous Return (VR) or Preload:
* It is the most important factor controlling the COP as the
heart adjust it self in order to keep COP equal to venous
return.
● Increase VR→↑EDV  SV
● Increase VR →↑HR
So, increase in both SV and HR leads to increase COP in order
to maintain balance between VR and COP.

15. CARDIAC OUTPUT
Mean Arterial Blood Pressure (Afterload):
Afterload is the force against which the heart is contracting
(aortic pressure).
When the mean arterial blood pressure is raised, the heart
pumps less amount of blood than it receives for several
beats so blood accumulates in the ventricles and the size
of the heart increases

16. Definition ,
Epidemiology
and Etiology
By : Ali Mansour Al Abbas

17. Definition :
Heart failure describes the clinical syndrome that develops
when:
The heart can not maintain adequate output or can do so
only at the expense of elevated ventricular filling pressure

18. In mild to moderate forms of heart failure : symptoms
occur only when the metabolic demand increases during
exercise or some other form of stress
In severe heart failure : symptoms may be present at rest

19. Epidemiology :
Heart failure is a major public health problem
Prevalence over 23 million worldwide
17.7 million died from cardiovascular diseases in 2015
7.4 million due to coronary heart disease
6.7 million due to stroke

22. Etiology :
Myocardial infraction
Coronary artery disease
Valve disease
Endocarditis
Myocarditis
Pericarditis
Pancarditis
Arrhythmias
Chronic hypertension
Thyroid disease
Septic shock
Idiopathic
Diabetes
Smoking
Alcohol and drugs addicted
Obesity
Pregnancy
Hypervolemia
High serum cholestrol

23. Pathogenesis of Heart
Failure
SAEED MOHAMMED BALARITH

24. Pathogenesis
– Ventricular dysfunction is the most
common cause of heart failure.
– This can occur because of impaired systolic
contraction, or diastolic dysfunction.
– This is most commonly found in patients
with left ventricular hypertrophy
– Abnormal ventricular relaxation due to a
stiff, non-compliant ventricle.

25. Pathogenesis
– Ventricular dysfunction
reduces cardiac output,
which, in turn, activates:
1)sympathetic nervous system
(SNS) and
2) renin–angiotensin–
aldosterone system (RAAS).
– lead to an increase in both
afterload and preload.

26. A vicious circle may
then be established
because any additional
fall in cardiac output
causes further
activation of the SNS
and RAAS, and an
additional increase in
peripheral vascular
resistance.

27. Pathogenesis
Neurohumoral activation and compensatory mechanisms in heart failure.
– Activation of the RAAS causes vasoconstriction and sodium and
water retention. This is mediated by angiotensin II, a potent
constrictor of arterioles
– Activation of the SNS also occurs and can initially sustain cardiac
output through increased myocardial contractility and heart rate.
– Prolonged sympathetic stimulation has negative effects, however,
causing cardiac myocyte apoptosis, cardiac hypertrophy and focal
myocardial necrosis.

28. TYPES OF HEART FAILURE
MOHAMMED MAJEED
ALWAILY

29. Systolic and diastolic heart failure
– Systolic and diastolic heart failure each result in a decrease in stroke volume.
– Systolic heart failure (pumping problem): inability of the heart to contract
enough to provide blood flow forwards
– Diastolic heart failure (filling problem): inability of the left ventricle to relax and
fill normally, resulting in fluid backing up into the lungs. .
– In systolic heart failure, the ejection fraction is reduced (HFrEF), because the
blood can’t be pumped out.
– In diastolic heart failure, the ejection fraction is preserved (HFpEF), because of
impaired filling.

33. Left heart failure
– This is characterised by a reduction in left ventricular output and
an increase in left atrial and pulmonary venous pressure.
– For example, in acute myocardial infarction – the rapid increase in
left atrial pressure causes pulmonary oedema. If the rise in atrial
pressure is more gradual (mitral stenosis), there is reflex
pulmonary vasoconstriction, which protects the patient from
pulmonary edema. However, the resulting increase in pulmonary
vascular resistance causes pulmonary hypertension, which in turn
impairs right ventricular function.

35. Biventricular heart failure
– In biventricular failure, both sides of the heart are
affected. This may occur because the disease process,
such as dilated cardiomyopathy or ischaemic heart
disease, affects both ventricles or because disease of the
left heart leads to chronic elevation of the left atrial
pressure, pulmonary hypertension and right heart
failure.

36. Right heart failure
– This is characterized by a reduction in right ventricular
output and an increase in right atrial and systemic
venous pressure.
– The most common causes are chronic lung disease,
pulmonary embolism and pulmonary valvular stenosis.
The term ‘cor pulmonale’ is used to describe right heart
failure that is secondary to chronic lung disease.

39. CLASSIFICATON OF HEART
FAILURE
AHMAD ABDULLAH
ALSHAREEF

40. INTRODUCTION
– Several constructs have been created for the purpose of
describing heart failure such that there is greater uniformity
in its diagnosis and treatment. The most common of these is
the New York Heart Association (NYHA) functional
classification that was first introduced in 1928 and still
persists due to its ease of use and clinical relevance.
– It places patients in one of four categories based on how
much they are limited during physical activity.

41. NYHA Class Patients with Cardiac Disease (Description of HF Related Symptoms)
Class I (Mild)
Patients with cardiac disease but without resulting in limitation of physical activity. Ordinary physical activity does
not cause undue fatigue, palpitation (rapid or pounding heart beat), dyspnea (shortness of breath), or anginal pain
(chest pain).
Class II (Mild)
Patients with cardiac disease resulting in slight limitation of physical activity. They are comfortable at rest. Ordinary
physical activity results in fatigue, palpitation, dyspnea, or anginal pain
Class III (Moderate)
Patients with cardiac disease resulting in marked limitation of physical activity. They are comfortable at rest. Less
than ordinary activity causes fatigue, palpitation, dyspnea, or anginal pain.
Class IV (Severe)
Patients with cardiac disease resulting in the inability to carry on any physical activity without discomfort. Symptoms
of heart failure or the anginal syndrome may be present even at rest. If any physical activity is undertaken,
discomfort is increased.

42. The American College of
Cardiology/American Heart Association
– The American College of Cardiology/American Heart
Association (ACC/AHA) staging system is defined by the
following four stage:
– Stage A: High risk of heart failure but no structural heart
disease or symptoms of heart failure (i.e. those with
diabetes, those with coronary disease).

43. CONT.
– Stage B: Structural heart disease but no symptoms
of heart failure. (i.e. reduced ejection fraction, left
ventricular hypertrophy, chamber enlargement).
– Stage C: Structural heart disease and symptoms of
heart failure.
– Stage D: Refractory heart failure requiring
specialized interventions.

44. ACCF/AHA Stage NYHA Functional Classification
Stage A
At high risk for HF but without
structural heart disease or symptoms of
HF
None
Stage B
Structural heart disease but without signs or
symptoms of HF Class I
No limitation of physical activity. Ordinary physical
activity does not cause symptoms of HF.
Stage C Structural heart disease with prior or current
symptoms of HF
Class II
Slight limitation of physical activity. Comfortable at rest,
but ordinary physical activity results in symptoms of HF.
Class III
Marked limitation of physical activity. Comfortable
at rest, but less than ordinary activity causes
symptoms of HF.
Stage D
Refractory HF requiring specialized
interventions Class IV
Unable to carry on any physical activity without
symptoms of HF, or symptoms of HF at rest.

45. clinical picture for Heart
Failure
Abulaziz Ibrahim Atef

46. Symptoms
– Abdominal swelling
– Dyspnea on exertion
– Edema
– Exercise intolerance
– Fatigue
– Orthopnea
– Paroxysmal nocturnal dyspnea
– Recent weight gain

47. Physical examination findings
– Abdomen: hepatojugular reflux, ascites
– Extremities: cool, dependent edema
– Heart: laterally displaced point of maximal impulse,
– S3 third heart sound (gallop or murmur)
– Lungs: labored breathing, pulmonary rales
– Retraction of chest wall

49. Physical examination findings
– Neck: elevated jugular venous pressure (distended)
– Skin: cyanosis, pallor
– Infants: The most common symptoms are :
– tachypnea and diaphoresis during feeds, easy fatigability,
irritability, decreased volume of feeds, and poor weight gain.
– delayed capillary refill

50. Crackles PulmonaryS3 sound gallop
S4 sound gallop

53. Criteria for Heart Failure

54. Framingham Diagnostic Criteria for Heart Failure
Major criteria
Acute pulmonary edema
Cardiomegaly
Hepatojugular reflex
Neck vein distension
Paroxysmal nocturnal dyspnea or orthopnea
Rales
Third heart sound gallop
Minor criteria
Ankle edema
Dyspnea on exertion
Hepatomegaly
Nocturnal cough
Pleural effusion
Tachycardia (> 120 beats per minute)
*—Heart failure is diagnosed when two major criteria or one
major and two minor criteria are met.

55. Boston Criteria for Diagnosing Heart
Failure
*— No more than 4 points are allowed from each of three categories; hence the
composite score (the sum of the subtotal from each category) has a possible
maximum of 12 points. The diagnosis of heart failure is classified as “definite” at a
score of 8 to 12 points, “possible” at a score of 5 to 7 points, and “unlikely” at a
score of 4 points or less.

56. Boston Criteria for Diagnosing Heart Failure
CRITERION POINT VALUE*
Category I: history
Rest dyspnea 4
Orthopnea 4
Paroxysmal nocturnal dyspnea 3
Dyspnea while walking on level area 2
Dyspnea while climbing 1
Category II: physical examination
Heart rate abnormality (1 point if 91 to 110 beats per minute; 2 points if more
than 110 beats per minute)
1 or 2
Jugular venous elevation (2 points if greater than 6 cm H2O; 3 points if greater
than 6 cm H2O plus hepatomegaly or edema)
2 or 3
Lung crackles (1 point if basilar; 2 points if more than basilar) 1 or 2
Wheezing 3
Third heart sound 3
Category III: chest radiography
Alveolar pulmonary edema 4
Interstitial pulmonary edema 3
Bilateral pleural effusion 3
Cardiothoracic ratio greater than 0.50 3
Upper zone flow redistribution 2

57. Differentiating Between Systolic and
Diastolic Dysfunction in Patients with
Heart Failure
X = suggestive;
— = not suggestive.

58. CLUES FROM THE EVALUATION SYSTOLIC DYSFUNCTION DIASTOLIC DYSFUNCTION
History Hypertension XX XXX
Coronary artery disease* XXX X
Diabetes mellitus XXX XX
Valvular heart disease* XXX —
Physical examination Third heard sound (S3) gallop* XXX X
Fourth heart sound (S4) gallop* X XXX
Rales XX XX
Jugular venous distention XX X
Edema XX X
Displaced point of maximal impulse* XX —
Mitral regurgitation* XXX X
Chest radiograph Cardiomegaly* XXX X
Pulmonary congestion XXX XXX
Electrocardiogram Q wave XX X
Left ventricular hypertrophy* X XXX
Echocardiogram Decreased ejection fraction* XXX —
Dilated left ventricle* XX —
Left ventricle hypertrophy* X XXX

60. Investigation
‫عقيل‬‫آل‬ ‫حمد‬‫يعقوب‬

61. Diagnosis of heart failure:
•Chest x-ray
• Assessment of LV function
•Echocardiogram
• Magnetic resonance imaging (MRI)
• Electrocardiogram
• Biomarkers
• Stress test
• Lab analysis heart failure

62. Chest X-ray:
Provides information about,
•Cardiac size and shape
•State of pulmonary vasculature (edema)
•Identify noncardiac cause of patient’s symptom
•Heart failure

64. •Assessment of LV function:
•2-D echocardiogram/Doppler
•Magnetic resonance imaging (MRI)

65. Echocardiogram:
•Non –invasive cardiac imaging is essential for the
diagnosis of heart failure.
•The must useful test is the two-dimentional(2-D).
•The echocardiogram/Doppler ,which can provide
assessment of left-ventricle size and function, valve
function and pericardial effusion

66. Magnetic resonance imaging (MRI):
•Analysis cardiac anatomy and function.
•Good standard for assessing left ventricle mass and volumes.
•Determining the cause of heart failure.

67. Normal
abnormal

69. Electrocardiogram (ECG):
is the record of all electrical activities (action potential) that occur
in all myocardial fibers during cardiac cycle.
•It is the single most useful test in evaluation of patient with heart
failure.
•Routine 12-leads electrocardiogram (ECG) Is recommended
•The major importance of ECG is assessing of cardiac rhythm and
determine of left ventricle hypertrophy

71. Ejection fraction:
Is important measurement in determining how well heart pumping out blood and
diagnosing and heart failure.
•The most useful index of left ventricle function.
•Easy to measure by noninvasive testing .
•Normal (>50%)-adequate systole function.
•Depressed (<30-40%)-contractility depressed.

72. Biomarkers:
•Adjunctive tools in diagnosis.
•Release from failing heart.
–
• With chronic heart failure, secrete increase amount of atria
natriuretic peptide (ANP) and brain natriuretic peptide (BNP).
•Usually is >400 pg/ml in patient with dyspnea due to heart failure.

73. Stress test:
•Stress test measure how the heart and blood vessel
response to exercise.
•Walk on treadmill/bicycle exercise.
•Through walk on treadmill attach with Electrocardiogram machine.
•Sometime patient can’t walk (do exercise) may receive the drugs
intravenously that stimulates heart similar to exercise.

75. Lab analysis heart failure:
•CBC:
Anemia can exacerbate heart failure.
•Fasting blood glucose
To evaluate for possible diabetes mellitus.
•Thyroid function tests .
Hypothyroidism can result in heart failure.
•Viral studies.
It viral infection (endocarditis, myocarditis, percarditis)

76. Complications of heart
failure
‫علي‬ ‫محمد‬ ‫عماد‬‫القحطاني‬

77. Several complications may occur in advanced heart failure, as
described below.
– Renal failure is caused by poor renal
perfusion due to low cardiac output and
may be exacerbated by diuretic therapy,
ACE inhibitors and angiotensin receptor
blockers (ARBs).

78. – Hypokalaemia may be the result of treatment with
potassium-losing diuretics or hyperaldosteronism caused by
activation of the renin–angiotensin system and impaired
aldosterone metabolism due to hepatic congestion. Most of
the body's potassium is intracellular and there may be
substantial depletion of potassium stores, even when the
plasma concentration is in the reference range.

79. – Hyperkalaemia may be due to the effects of drugs that
promote renal resorption of potassium, in particular the
combination of ACE inhibitors, ARBs and mineralocorticoid
receptor antagonists. These effects are amplified if there is
renal dysfunction due to low cardiac output or
atherosclerotic renal vascular disease.

80. – Hyponatraemia is a feature of severe heart failure
and is a poor prognostic sign. It may be caused by
diuretic therapy, inappropriate water retention due
to high vasopressin secretion, or failure of the cell
membrane ion pump.

81. – Impaired liver function is caused by hepatic venous
congestion and poor arterial perfusion, which frequently
cause mild jaundice and abnormal liver function tests;
reduced synthesis of clotting factors can make
anticoagulant control difficult.

82. – Thromboembolism . Deep vein thrombosis and pulmonary
embolism may occur due to the effects of a low cardiac
output and enforced immobility. Systemic emboli occur in
patients with atrial fibrillation or flutter, or with
intracardiac thrombus complicating conditions such as
mitral stenosis, MI or left ventricular aneurysm.

83. – Sudden death occurs in up to 50% of patients with heart
failure and is most probably due to ventricular fibrillation.

84. References

85. References
– https://emedicine.medscape.com/article/163062-overview
– https://bestpractice.bmj.com/topics/en-us/61
– https://www.escardio.org/Guidelines/Clinical-Practice-Guidelines/Acute-and-
Chronic-Heart-Failure
– https://www.aafp.org/afp/2000/0301/p1319.html
– http://www.heart.org/en/health-topics/heart-failure/warning-signs-of-heart-failure
– https://www.uptodate.com/contents/clinical-manifestations-and-diagnosis-of-
advanced-heart-
failure?search=Heart%20Failure&source=search_result&selectedTitle=2~150&usage
_type=default&display_rank=2