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Congestive Heart Failure

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Objectives

• Define heart failure and discuss the etiology


• Discuss the classification of heart failure.
• Compare the pathophysiology of left and right
heart failure
• Discuss the compensatory mechanisms involved in
cardiac failure:
– sympathetic nervous system activation;
– neuro-endocrine response;
– dilation;
– Hypertrophy

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Objectives
• Discuss the likely investigations that may be performed.
• Discuss the collaborative management (including
pharmacological) of the patient with cardiac failure
• Briefly discuss the action of the following pharmacological
agents used to treat heart failure:
– Diuretics
– ACE inhibitors
– Digoxin
– Beta blockers
– Positive inotropic agents
– Anticoagulants

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Definition

 “state in which the heart fails to meet various


oxygen and metabolic needs of the body under
differing circumstances” (Sokolow, & McIlroy,
1993, p. 120)
 Multi-system disorder characterised by
abnormalities of cardiac, skeletal muscle, and renal
function, stimulation of sympathetic nervous
system, and a complex pattern of neurohormonal
changes (Jackson, Gibbs, Davies and Yip, 2000)
 CHF is an abnormal condition involving impaired
cardiac pumping

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Classification

• Backward and forward failure


– You need to know gross anatomy!
• Acute and chronic failure
– New, old, new on old
• Right and left sided failure
– Again, you need to know your anatomy
• Compensated or decompensated
– In other words is the body coping or failing

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Pulmonary
The Heart Left atrial filling
circulation AORTA From pulmonary circ
Left lung PA->2
Oxygen rich
Right lung
Left lung
PV->2 Right lung

.
VC

Venous return .
RA
LA

IVC, SVC, AV Valve BI


jugular veins

LV
Liver Systemic circulation
RV
Blood pressure as we
AV valve TRI measure it
Consider the word MAP

Semi Semi
Lunar Lunar
TRI TRI 6
Aetiology 1
• Abnormal volume load
• too much circulating volume
• Abnormal pressure load
• poor pump or narrow
• Myocardial dysfunction
• Dysrythmias, AMI, heart cell damage
• hypovolaemia, poor return
• Increased metabolic demands
• Infection, condition of failure in progress so increased HR
and increased WOB

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Aetiology 2

• Western countries
– Coronary artery disease
– Hypertension
• Developing countries
– Valvular disease
– Nutritional cardiac disease
• Other causes
– Cardiomyopathies
– Pericardial disease
– Arrhythmias
– High output failure – anaemia, arrhythmias
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Precipitating Causes of Insufficiency

• Progression of underlying heart disease


• Anaemia
• Change in therapy or cessation of therapy
• Arrhythmia
• Pulmonary embolism
• Fluid or sodium overload

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Pathophysiology

• Not just pump inadequacy responsible for syndrome


• Normally primary event is reduction in myocytes (heart
muscle cells)
• A number of compensatory mechanism s initially help
maintain cardiac output and peripheral perfusion
• These mechansims have long term consequences

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Compensatory Mechanisms

Compensatory mechanism

Ventricular Ventricular Activation of Neurohormonal


Dilatation Hypertrophy SNS response

-Enlargement of - The muscle & • Inadequate SV Inadequate CO


the chamber of cardiac wall  & CO  stimulate kidney
the heart contractile activation SNS release renin 
-The muscle •Increased Nor & RAA system
fiber of the heart CO increased adrenalin
stretch  (increased HR,
increased contractility &
contractility peripheral
CO vasocontsriksi)

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Compensatory Mechanisms: Sympathetic
Nervous System Response

Figure 21-1 Clochesy, Breu, Cardin, Whittaker, and Rudy, 1996,


Critical care nursing, p. 383
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Compensatory Mechanisms: Renal
Compensation

Figure 21-2 Clochesy, Breu, Cardin, Whittaker, and


Rudy, 1996, Critical care nursing, p. 385
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Impaired Ventricular Function

 cardiac output

Neuro-Endocrine systems RAA system

 HR vasoconstriction fluid retention

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Clinical Features 1

• Subjective
– Dyspnoea
– Orthopnoea
– Paroxysmal nocturnal dyspnoea
– Reduced exercise tolerance
– Palpitations
– Fatigue and weakness
– Weight gain

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Clinical Features 2

• Objective
– Tachycardia
– Elevated JVP
– Crackles and wheezes
– Pleural effusion
– Extra heart sounds
– Altered haemodynamic measurements
– Oedema

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Elevated JVP The Heart Left atrial filling
Up here AORTA From pulmonary circ
PA->2
Oxygen rich
Increased
pressure here Left lung
PV->2 Right lung

.
VC

Venous return .
RA
LA

IVC, SVC, AV Valve BI


jugular veins
Liver, legs
LV
RV Systemic circulation
Blood pressure as we
AV valve TRI measure it
Venous Consider the word MAP
congestion in
liver, legs down Semi Semi
here Lunar Lunar
TRI TRI 17
Failure of right side

• Caused by failing left side


• Obstruction in pulmonary circulation eg PE
• AMI effecting right side of heart

• Forwards; impaired ability to pump blood into


pulmonary circulation

• Backwards; effects on vessels and organs preceding


right side of heart.

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The Heart Back pressure up here

AORTA May cause APO


PA->2 Left atrial filling
From pulmonary circ
Oxygen rich
PV->2

.
VC Left lung

.
Right lung

Venous return LA

IVC, SVC, RA AV Valve BI


jugular veins
Liver, legs Failing ventricle here
LV
RV Poor organ perfussion seen here
Eg decreased urine output
Low BP, decreased concious state
AV valve TRI
Systemic circulation
Blood pressure as we
Semi Semi measure it
Lunar Lunar Consider the word MAP
TRI TRI 19
Failure of left side
• Backwards
• Build up of pressure in pulmonary circulation
• Effecting oxygenation of blood
• May progress to right side of heart as described 2 slides
ago because right side will have increased pressure to
push against

• Forwards
• Poor organ perfusion
• Decreased urine output
• Decreased systemic blood pressure MAP 60mmHg

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Clinical Features 3: Complications

• Arrhythmias
• Thromboembolism
• Hepatic congestion and dysfunction
• Muscle wasting
• Respiratory muscle weakness

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Presentation of Acute Pulmonary
Oedema

• Dyspnoeic
• Tachypnoeic
• Pale
• Sweaty
• Anxious
• Confused
• Won’t lie flat

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Investigations : Initial

• Chest x-ray
• 12-lead ECG
• Urea and electrolytes
• Haematology
• CK and Troponin if suspect AMI

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Investigations: Ongoing

• Exercise test
• Coronary angiogram
• echocardiogram
• Pulmonary function tests

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Goal of Treatment

• Aim is to
– Reduce mortality
– Manage symptoms
– Enhance self-management
• Improve in functional capacity
– Quality of life
– ? Degree of improvement in quantity
(length)

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Steps to Determine Treatment 1

 Establish cause
– e.g. IHD, HT, valve disease

 Provide treatment for primary defect


– Revascularisation
– Anti-hypertensives
– Valve surgery

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Steps to Determine Treatment 2

 Define the syndrome


– Acute or chronic
– Backward or forward
– Right sided or left sided failure

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Pulmonary
The Heart Left atrial filling
circulation AORTA From pulmonary circ
Left lung PA->2
Oxygen rich
Right lung
Left lung
PV->2 Right lung
VC

Venous return LA

IVC, SVC, RA AV Valve BI


jugular veins

LV
Liver Systemic circulation
RV
Blood pressure as we
AV valve TRI measure it
Consider the word MAP

Semi Semi
Lunar Lunar
TRI TRI 28
Steps to Determine Treatment 3

 Identify / Correct precipitating causes


– Prevent progression of ischaemia
– Non-compliance with medications
– Infection
– Anaemia
– Diet/exercise
– Sleep apnoea

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Treatment - Asymptomatic

 Risk factor reduction


– Smoking, obesity, hypertension
 ACE inhibitor
– Prevent sodium and water retention and
vasoconstriction caused by activation of RAA
– Early and long term use post AMI
– Associated with a delay in heart failure symptoms
– Prevents ventricular dilatation
– Reduces work of the heart by  preload and 
afterload
– Increase ejection fraction

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Treatment – Symptomatic
• Risk factor modification
• ACE Inhibitor
• Diuretics
– Symptom relief
– Loop diuretics increase urinary sodium and chloride
excretion in ascending limb of loop of Henle
– Thiazides for mild failure – act on distal convoluted
tubule
– Loop diuretics for severe failure
– Dose adjusted to fluid state / weight

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Treatment – Symptomatic

• -blockers
– e.g. carvedilol, metoprolol, bisoprolol
– Block effects of sympathetic activity
–  HR,  myocardial ischaemia,  arrhythmia
– myocardial perfusion
– All patients with chronic stable mild to moderate
failure

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Treatment - Symptomatic

 ? Digoxin
–   HR + mild  contractility
– Useful for controlling rate AF
– Multiple side effects – narrow
therapeutic window (nausea,
arrhythmias, confusion)
• May prevent clinical worsening
• May improve symptoms in chronic failure

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Treatment – Symptomatic

• ? Anticoagulants
–Warfarin if in AF or thrombus
formation likely
–Aspirin if history of IHD

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Treatment – Refractory Heart Failure

 Intravenous inotrope
–Dobutamine
–Noradrenalin
 Implantable defibrillator
 Biventricular pacing
 Intra-Aortic Balloon Pump
 LV Assist Device
 Cardiac Transplantation

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