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Heart Failure

Definition
• The inability of the cardiovascular system to meet the demands of the
end organs
• Heart failure may result from abnormal contractile function (systolic
dysfunction) or impaired relaxation (diastolic dysfunction).
• Diastolic dysfunction is defined as clinical heart failure syndrome with
normal LV systolic function on cardiac testing.
Etiology
• Cardiac failure is the leading cause of hospitalization in people older
than 65 and it is associated with an annual mortality rate of 10%.
• The most common cause of cardiac failure is IHD but there are many
others
Diagnosis
• Heart failure is diagnosed clinically and by chest radiography
(cardiomegaly), echocardiography, ECG and biochemistry.

• Echocardiography determines :
• The troke volume (SV; the amount of blood that exits the ventricles with each
heartbeat)
• The end-diastolic volume (EDV; the amount of blood at the end of diastole)
• The SV in proportion to the EDV (the ejection fraction; EF).
• Normally, the EF should lie between 50 and 70% but, in cardiac failure, it is <
40%.
Clinical Features
• Features depend on which side of the heart, left or right, is
predominantly involved and on the type of failure, either diastolic or
systolic.
• Symptoms can be few until activity becomes limited with
breathlessness (dyspnoea), cyanosis and dependent oedema (usually
swollen ankles or sacral oedema)
Left-sided Heart Failure
• Results in damming of blood back from the left ventricle to the
pulmonary circulation with pulmonary hypertension, pulmonary
oedema and dyspnoea
Right-sided Heart Failure
• Causes congestion of the main venous systems and thus affects
primarily the liver, gastrointestinal tract, kidneys and
subcutaneous tissues
• The American College of Cardiology/American Heart Association has
defined four stages in the progression of cardiac failure
Management
• Heart failure is managed by treating the symptoms and signs by
reducing the heart workload, and correcting precipitating factors such
as hypertension, anaemia, valvular disease and thyrotoxicosis.

• General measures may include rest, stress reduction, control of


hypertension, weight loss, stopping smoking, and salt restriction.
First Line Therapy
• Angiotensin-converting enzyme inhibitors (ACEi; such as
enalapril, ramipril, quinapril, perindopril, lisinopril and
benazepril)
• Angiotensin II receptor blockers or sartans (e.g. valsartan,
telmisartan, losartan, irbesartan and olmesartan)

• delaying progression of failure and reducing mortality


• improve myocardial contractility, tissue and organ perfusion and
oxygenation.
• Diuretics (mainly loop diuretics such as furosemide or bumetanide) 
increase sodium and water excretion.
• Betablockers  for patients with systolic heart failure due to left
ventricular systolic dysfunction after stabilization with ACEi and diuretics.
• Recombinant BNP (nesiritide)  for patients with acute heart failure who
have dyspnoea at rest.
• Antagonists of vasopressin receptor (tolvaptan and conivaptan) and
aldosterone receptor (spironolactone and eplerenone)  newer therapies.
• Phosphodiesterase inhibitors (enoximone or milrinone)  support cardiac
function.
• Digoxin may help when failure is associated with atrial fibrillation.
Dental Aspects
• Emergency dental care should be conservative, principally with
analgesics and antibiotics.
• Routine dental care can usually be provided for patients with mild
controlled cardiac failure with little modification.
• Appointments for patients with cardiac failure should be short and in
the late morning.
• The dental chair should be kept in a partially reclining or erect
position  It is dangerous to lay any patient with left-sided heart
failure supine, as this may severely worsen dyspnoea.
• Lidocaine or prilocaine can be used but bupivacaine should be
avoided as it is cardiotoxic.
• Adrenaline/epinephrine may theoretically increase hypertension and
precipitate arrhythmias.
ARRHYTHMIAS
Definition
• Abnormalities of cardiac rhythm can be broadly defined as any
deviation from the normal cardiac pacemaker and conduction
mechanism.
• Tachyarrhythmias  increased automaticity of cardiac pacemaker cells’ re-
entry or triggered activity and are defined as any abnormal heart rhythm with
a rate > 100 bpm.
• Bradyarrhythmias  result of sinoatrial node dysfunction and conduction
block at any level of the conduction tissues, including the atrioventricular
node, His- Purkinje system, or distal branches of the left and right bundles.
• Bradyarrhythmias  heart rates of < 60 bpm.
• Both tachyarrhythmias and bradyarrhythmias may be hemodynamically well
tolerated in patients with normal cardiac function, or they may result in
cardiovascular collapse if cardiac output is significantly compromised.
Sinoatrial (SA) node

Atrioventricular (AV) Node

Bundle of His

Right and Left bundle


branches

subendocardial Purkinje
network
Etiology
Classification
• Arrhythmias classified by rate :

• Heart rate > 100 beats/ minute


• It may result in palpitation, but is not
Tachycardias necessarily an arrhythmia.

• Heart rate < 60 beats/minute


• caused by a slowed electrical signal from the
Brachycardias SA node (sinus bradycardia), a pause in the
normal activity of the SA node (sinus arrest),
or blocking of the impulse between the atria
and ventricles (AV block or heart block)
Tachycardias

• Supraventricular tachycardias
Arrhythmia that arises above the bifurcation of the His bundle into
right and left bundle branches

Triggered activity is caused by after-depolarizations that reach activation


threshold. This can be a mechanism for atrial and ventricular arrhythmias. It is
related to the flow of calcium in and out of cells and sometimes responds to
calcium-channel blockers.
Atrioventricular nodal re-entrant tachycardia is the most common cause of
paroxysmal supraventricular tachycardia (PSVT) and occurs most often in
young people and infants.
• Ventricular tachycardias
Usually the result of structural heart disease, most commonly related
to previous myocardial infarction and is dangerous as it can result in
chest pain, cardiac failure, syncope or ventricular fibrillation.

Ventricular fibrillation is the most serious arrhythmia and the most common
cause of sudden death.
 Typically a consequence of myocardial infarction or structural heart disease,
occasionally of idiopathic fibrosis affecting the conduction mechanism,
thyrotoxicosis, halothane anaesthesia, or adrenaline/epinephrine, cocaine or
digitalis overdosage.
Ventricular fibrillation is effectively a type of cardiac arrest and is imminently
life threatening.
Brachycardias

• Bradycardia may be unimportant in a young person and is often found


in athletes.
• Bradycardia in an older person, however, especially when associated
with heart disease, can cause sudden loss of consciousness (syncope).
Management
• Catheter ablation is the treatment of choice for most simple arrhythmias
and also has an important role with more complex rhythm disorders (e.g.
atrial fibrillation and ventricular tachycardia).
• Electric shock across the heart (defibrillation or cardioversion), either
externally to the chest or internally to the heart via implanted electrodes,
may be needed.
• Defibrillation is the application of a shock that is not synchronized; it is
needed for the chaotic rhythm of ventricular fibrillation and for pulseless
ventricular tachycardia.
• Defibrillation or cardioversion may also be accomplished by an automatic
implantable cardioverter–defibrillator, an electronic device that is the most
successful treatment to prevent ventricular fibrillation and 99% effective in
stopping lifethreatening arrhythmias.
• Bradycardias may be treated by cardiac pacing with a pacemaker – a small
implanted electronic device which has a pulse generator and one
(monopolar) or, more usually now, two (bipolar) electrode leads and is
powered by lithium batteries.
Dental Aspects
• Some dental electrical devices capable of generating electromagnetic
radiation may pose a low-grade threat to dental patients but usually
only if the devices are placed very close to the pacemaker.
• Pacemaker single-beat inhibition of little consequence may
occasionally be caused by dental equipment such as ultrasonic scalers
and ultrasonic baths, older ferromagnetic ultrasonic scalers, pulp
testers, electronic apex locators, dental induction casting machines,
belt-driven motors in dental chairs, and older radiography machines.
• Several anti-arrhythmic drugs can
cause oral lesions.
• Verapamil, enalapril and diltiazem 
gingival hyperplasia,
• Beta-blockers  lichenoid ulceration
• Procainamide  lupus-like reaction.
• Patients with pacemakers are
usually advised to avoid elective
dental care within the first few
weeks after receiving the
pacemaker.