2. • Aberrant rhythms can be initiated anywhere
in the conduction system, from the sinoatrial
(SA) node down to the level of an individual
myocyte; they are typically designated as
originating from the atrium
(supraventricular) or within the ventricular
myocardium. Abnormalities in myocardial
conduction can be sustained or sporadic
(paroxysmal).
3. • They can manifest as tachycardia (fast heart
rate), bradycardia (slow heart rate), an irregular
rhythm with normal ventricular contraction,
chaotic depolarization without functional
ventricular contraction (ventricular fibrillation), or
no electrical activity at all (asystole).
• Patients may be unaware of a rhythm disorder, or
may note a “racing heart” or palpitations
(irregular rhythm); loss of adequate cardiac
output due to sustained arrhythmia can produce
lightheadedness (near syncope), loss of
consciousness (syncope), or sudden cardiac death
4. • Ischemic injury is the most common cause of rhythm
disorders, either through direct damage or through
the dilation of heart chambers that alters signal
conduction.
• If the SA node is damaged (e.g., sick sinus syndrome),
other fibers or even the atrioventricular (AV) node can
take over pacemaker function, albeit at a much slower
intrinsic rate (causing bradycardia).
• If the atrial myocytes become “irritable” and depolarize
independently and sporadically (as occurs with atrial
dilation), the signals are variably transmitted through
the AV node leading to the random “irregularly
irregular” heart rate of atrial fibrillation.
5. • If the AV node is dysfunctional, varying
degrees of heart block occur, ranging from
simple prolongation of the P-R interval on the
ECG (first-degree heart block), to intermittent
transmission of the signal (second-degree
heart block), to complete failure (third-degree
heart block).
6. Sudden Cardiac Death
• Sudden cardiac death (SCD) is defined as
unexpected death due to a lethal arrhythmia
such as asystole or sustained ventricular
fibrillation.
• The prognosis of many patients at risk for SCD,
including those with chronic IHD, is markedly
improved by implantation of a pacemaker or an
automatic cardioverter defibrillator, which senses
and electrically counteracts an episode of
ventricular fibrillation.
7. HYPERTENSIVE HEART DISEASE
• Hypertensive heart disease (HHD) is a
consequence of the increased demands
placed on the heart by hypertension, causing
pressure overload and ventricular
hypertrophy.
9. Systemic (Left-Sided) Hypertensive
Heart Disease
• The criteria for the diagnosis of systemic
hypertensive heart disease are (1) left
ventricular hypertrophy in the absence of
other cardiovascular pathology (e.g., valvular
stenosis), and (2) a history or pathologic
evidence of hypertension.
10. Clinical Features
• Compensated HHD typically is asymptomatic
and is suspected only from discovery of
elevated blood pressure on routine physical
examination, or from ECG or
echocardiographic findings of left ventricular
hypertrophy. In some patients, the disease
comes to attention with the onset of atrial
fibrillation (secondary to left atrial
enlargement) and/or CHF.
11. Pulmonary Hypertensive Heart Disease—
Cor Pulmonale
• Cor pulmonale consists of right ventricular
hypertrophy and dilation—frequently
accompanied by right-sided heart failure—
caused by pulmonary hypertension attributable
to primary disorders of the lung parenchyma or
pulmonary vasculature.
• Cor pulmonale can be acute in onset, as with
pulmonary embolism, or can have a slow and
insidious onset when due to prolonged pressure
overload in the setting of chronic lung and
pulmonary vascular disease
12. VALVULAR HEART DISEASE
• Valvular disease may result in stenosis,
insufficiency (regurgitation or incompetence),
or both.
• • Stenosis is the failure of a valve to open
completely, obstructing forward flow. Valvular
stenosis is almost always due to a primary
cuspal abnormality stemming from a chronic
process (e.g., calcification or valve scarring).
13. • Insufficiency results from failure of a valve to
close completely, thereby allowing regurgitation
(backflow) of blood. Valvular insufficiency can
result from either intrinsic disease of the valve
cusps (e.g., endocarditis) or disruption of the
supporting structures (e.g., the aorta, mitral
annulus, tendinous cords, papillary muscles, or
ventricular free wall) without primary cuspal
injury. It can appear abruptly, as with chordal
rupture, or insidiously as a consequence of leaflet
scarring and retraction.
