Congestive Cardiac Failure

Congestive Cardiac Failure
Imtiyaz Ali
Lecturer, UTAR
Objectives
 Define CCF
 Understand pathomechanism &
pathophysiology of CCF
 Discuss about etiology of CCF
 Describe clinical symptoms of CCF
 Know the diagnostic procedures of CCF
 Understand the medical treatment of CCF
 Explain acute decompensated heart failure,
its causes, clinical features and treatment
 Clinical syndrome that results from any
structural or functional cardiac disorder in
which heart is unable to pump adequate
amount of blood to meet metabolic needs
 Does not mean the heart has failed, simply
means the heart is not doing an efficient job
 Congestive Heart Failure affects people of all
ages from children to senior citizens, there is
no cure
 One or both of ventricles can no longer work as hard as they
used to, pumping blood insufficient for body’s needs
 The right side of the heart collects the blood returning from the
body and sends it to the lungs
 If it is failing, the blood backs up into the veins, and there are
signs of edema
 The left side of the heart receives the blood from the lungs and
pumps it out into the body
 If it is failing the blood is not pumped effectively causing
decreased cardiac output
Factors Affecting Cardiac Output
Preload
Cardiac Output = Heart Rate X Stroke Volume
Afterload Contractility
Pathomechanisms involved in heart
failure
 Cardiac mechanical dysfunction can develop as a
consequence in preload, contractility and afterload disorders
 Disorders of preload
 preload  length of sarcomere is more than optimal 

  strength of contraction
 preload  length of sarcomere is well below the optimal 

  strength of contraction
failure
 Disorders of contractility
In the most forms of heart failure the contractility of myocardium is

decreased (ischemia, hypoxia, acidosis, inflammation, toxins, metabolic
disorders)
• Disorders of afterload due to:
• fluid retention in the body
•  arterial resistance
• valvular heart diseases ( stenosis )

failure
Pathophysiology of CCF
 Pump fails → decreased stroke volume /CO
 Compensatory mechanisms kick in to increase
CO
◦ SNS stimulation → release of epinephrine/nor-
epinephrine
 Increase HR
 Increase contractility
 Peripheral vasoconstriction (increases afterload)
◦ Myocardial hypertrophy: walls of heart thicken to
provide more muscle mass → stronger contractions
◦ Hormonal response: ↓ renal perfusion interpreted by
juxtaglomerular apparatus as hypovolemia, thus:
 Kidneys release renin, which stimulates conversion of
angiotensin I → angiotensin II, which causes:
 Aldosterone release → Na retention and water
retention (via ADH secretion)
 Peripheral vasoconstriction
 Compensatory mechanisms may restore CO
to near-normal
 But, if excessive the compensatory
mechanisms can worsen heart failure because
......
Pathophysiology of CHF
 Vasoconstriction: ↑’s the resistance against which
heart has to pump (i.e., ↑’s afterload), and may
therefore ↓ CO
 Na and water retention: ↑’s fluid volume, which ↑’s

preload. If too much “stretch” (d/t too much fluid) →
↓ strength of contraction and ↓’s CO
 Excessive tachycardia → ↓’d diastolic filling time →

↓’d ventricular filling → ↓’d SV and CO
Risk Factors
 Interference with normal mechanisms regulating
cardiac output
◦ HTN
◦ Myocardial infarction
◦ Dysrhythmias
◦ Valvular disorders
◦ CAD
◦ Age
◦ Obesity
◦ Cigarette smoking
◦ Diabetes mellitus
◦ High cholesterol
◦ African descent
Types of Congestive Cardiac Failure
 Low-Output Cardiac Failure
◦ Systolic Heart Failure:
 decreased cardiac output
 Decreased Left ventricular ejection fraction
◦ Diastolic Heart Failure:
 Elevated Left and Right ventricular end-diastolic pressures
 May have normal LVEF
 High-Output Cardiac Failure
 Seen with peripheral shunting, low-systemic vascular
resistance, hyperthryoidism, anemia
 Often have normal cardiac output
 Left-sided failure
 Most common form
 Blood backs up through the left atrium into the
pulmonary veins
 Pulmonary congestion and edema
 Eventually leads to biventricular failure

 Left-sided failure
◦ Most common cause:
 HTN
 Cardiomyopathy
 Valvular disorders
 CAD (myocardial infarction)
 Right-sided failure
 Results from diseased right ventricle
 Blood backs up into right atrium and venous
circulation
 Causes
 LVF (Left ventricular failure)
 Corpulmonale (Right ventricular dilation and
hypertrophy caused by pulmonary pathology)
 RV infarction
 Right-sided failure
 Venous congestion
 Peripheral edema
 Hepatomegaly
 Splenomegaly
 Jugular venous distension
Clinical Manifestations
 Pulmonary edema
 Agitation
 Pale or cyanotic
 Cold, clammy skin
 Severe dyspnea
 Tachypnea
 Pink, frothy sputum
 Fatigue
 Dyspnea
◦ Paroxysmal nocturnal dyspnea (PND)
 Tachycardia
 Edema – (lung, liver, abdomen, legs)
 Nocturia
 Behavioral changes
◦ Restlessness, confusion,  attention span
 Chest pain (d/t  CO and ↑ myocardial work)
 Weight changes (r/t fluid retention)
 Skin changes
◦ Dusky appearance
Classification of heart failure
 New York Heart Association (NYHA) Functional Classification
Class % of patients Symptoms
I 35% No symptoms or limitations in ordinary physical activity
II 35% Mild symptoms and slight limitation during ordinary activity
III 25% Marked limitation in activity even during minimal activity.

Comfortable only at rest
IV 5% Severe limitation. Experiences symptoms even at rest

Classification of heart failure
 Based on the person’s tolerance to physical
activity
 Class 1: No limitation of physical activity
 Class 2: Slight limitation
 Class 3: Marked limitation
 Class 4: Inability to carry on any physical activity without
discomfort
Diagnosis
 Primary goal is to determine underlying cause
 Physical exam
 Chest x-ray
 ECG
 Hemodynamic assessment
 Echocardiogram
 Cardiac catheterization
Chest X-ray in Heart Failure
 Cardiomegaly
 Cephalization of the pulmonary vessels
 Pleural effusions
Echocardiogram
 Uses ultrasound to visualize myocardial structures and
movement
 calculate EF
Cardiac catheterization
Management
 Primary goal is to improve LV function by:
◦ Decreasing intravascular volume
◦ Decreasing venous return
◦ Decreasing afterload
◦ Improving gas exchange and oxygenation
◦ Improving cardiac function
◦ Reducing anxiety
Management
 Decreasing intravascular volume
◦ Improves LV function by reducing venous
return
◦ Loop diuretic: drug of choice
 Reduces preload
◦ High Fowler’s position
High Fowler’s position
Management
 Decreasing afterload
◦ Drug therapy:
 Vasodilation (ACE inhibitors)
 Decreases pulmonary congestion
Management
 Improving cardiac function
◦ Positive inotropes
 Improving gas exchange and oxygenation
◦ Administer oxygen, sometimes intubate and
ventilate
 Reducing anxiety
◦ Morphine
Collaborative Care
 Treat underlying cause
 Maximize CO
 Alleviate symptoms
 Oxygen treatment
 Rest
 Biventricular pacing
 Cardiac transplantation
Biventricular pacing
Drug Therapy
 ACE inhibitors
 Diuretics
 Inotropic drugs
 Vasodilators
 -Adrenergic blockers
Acute Decompensated Heart Failure
 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
 Causes:
Acute MI
 Rupture of chordae tendinae/acute mitral valve insufficiency
Volume Overload
 Transfusions, IV fluids
 Non-compliance with diuretics, diet (high salt intake)
Worsening valvular defect
 Aortic stenosis
Decompensated Heart Failure
 Symptoms
◦ Severe dyspnea
◦ Cough
 Clinical Findings
◦ Tachypnea
◦ Tachycardia
◦ Hypertension/Hypotension
◦ Crackles on lung exam
◦ New murmur
Decompensated Heart Failure
 Treatment
◦ Oxygen, mechanical ventilation if needed
◦ Loop diuretics (Lasix!)
◦ Morphine
◦ Vasodilator therapy (nitroglycerin)

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Congestive Cardiac Failure

Cardiac Output = Heart Rate X Stroke Volume

 preload  length of sarcomere is more than optimal 

 preload  length of sarcomere is well below the optimal 

In the most forms of heart failure the contractility of myocardium is

• Disorders of afterload due to:

• fluid retention in the body

• valvular heart diseases ( stenosis )

 Na and water retention: ↑’s fluid volume, which ↑’s

 Excessive tachycardia → ↓’d diastolic filling time →

 Eventually leads to biventricular failure

Class % of patients Symptoms

I 35% No symptoms or limitations in ordinary physical activity

II 35% Mild symptoms and slight limitation during ordinary activity

III 25% Marked limitation in activity even during minimal activity.

IV 5% Severe limitation. Experiences symptoms even at rest

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