Congestive heart failure

Congestive heart failure (CHF/CCF) may be

defined as the pathophysiological state
resulting from impaired cardiac function,
rendering the heart unable to maintain a
cardiac output sufficient for the metabolic
requirements of tissue & organs of the body.
CHF may occur either
i) by the decreased myocardial capacity to
contract or
ii) due to an increased pressure stroke-
volume imposed on the heart.
CCf may involve the right ventricle, left
ventricle or both. The ventricular dysfunction
may be systolic (i.e. inadequate force of
contraction to eject blood normally) or
diastolic (i.e. inadequate relaxation to permit
normal feeling).
Systolic dysfunction often occurs with
ischemic injury, or
volume overload, or
dilated cardiomyopathy.
Diastolic dysfunction occur with
massive left ventricular hypertrophy,
myocardial fibrosis,
deposition of amyloid or
constrictive pericarditis.
Whatever its basis , CCF is characterized by
diminished cardiac output or damming back of
blood in the venous system or both.
The primary sign and symptoms of all types of
CCF include tachycardia, decreased exercise
tolerance, shortness of breath(due to
pulmonary congestion), peripheral and
pulmonary edema and cardiomegaly.
Decreased exercise tolerance with rapid
muscular fatigue is the major direct
consequence of diminished cardiac output.
Decreased CO again stimulates the
compensatory sympathetic outflow and renin-
angiotensin system.
Increased sympathetic outflow causes
increased cardiac contractility, increased
heart rate, increased preload, increased
vascular tone.
While increased preload, force and heart rate
initially increase CO but increased arterial tone
results in increased afterload (arterial
resistance) and decreased ejection fraction, CO
and renal perfusion. Increased angiotensin II
production leads to increased aldosterone
secretion( with Na & water retension),
increased afterload(vasoconstrictio), and
remodeling of both heart and vessels.
The most important intrinsic compensatory
mechanism is myocardial hypertrophy. This
increased muscle mass (contractile
apparatus) helps to maintain cardiac
performance at the face of adverse effects such
as pressure or volume overload, loss of
functional tissue(MI) and decrease in cardiac
contractility. However after an initial
beneficial effect, hypertrophy can lead to
ischemic change, impairment of diastolic
feeling and ultimately cardiac failure.
 CO

↓Carotid sinus firing ↓Renal blood flow

↑Sympathetic discharge ↑Renin release

↑ Angiotensin II

↑Force

↑Rate

↑Preload ↑Afterload Remodeling

↑CO via compensation
 Left sided heart failure
Left sided heart failure most often caused by –
 Ischemic heart disease
 Hypertension
 Aortic and mitral valvular disease
 Myocardial disease
In left sided heart failure left ventricle is
usually hypertrophied and often dilated,
sometimes quite massively. Secondary
enlargement of the atrium is frequently
present. Atrial fibrillation often results.
The distant effects of left sided failure are
manifestated most prominently in the lungs,
although the function of the kidney and brain
may also be markedly impaired.
 Right-sided heart failure
Right-sided heart failure occurs in pure form
is only in few diseases. Usually it is a
consequence of left sided failure because any
increases in pressure in pulmonary circulation
inevitably produces an increased burden on the
right side of the heart. The causes of right
sided heart failure is then must include all
those that induce left sided heart failure.
Pure right sided failure most often occurs
when right ventricle is overloaded with blood
that is induced by intrinsic disease of the
lungs or the pulmonary vasculature.
Hence, the right ventricle is burdened by
increased resistance within the pulmonary
circulation. Dilatation is generally confined to
the right ventricle and atrium. The major
organs affected by the right sided heart failure
are liver, spleen, kidneys, subcutaneous
tissues, brain as well as the entire portal area
of the venous drainage.
Types of heart disease
Four categories of heart diseases are
responsible for about 85-90% of all cardiac
death—
1. Ischemic heart disease
2. Hypertensive heart disease and pulmonary
hypertensive heart disease(cor pulmonale)
3. Certain valvular disease such as calcefic
aortic valve stenosis, mitral valve prolapse,
infective endocarditis and rheumatic heart
disease
4. Congenital heart disease
 Ischemic heart disease (IHD)
IHD is a group of closely related syndrome
resulting from ischemia. Ischemia means lack
of blood supply.
Ischemia consists of not only insufficiency of
oxygen but also reduced availability of
nutrient substrates and inadequate removal of
metabolites.
Ischemia occurs due to an imbalance between
the supply and demand of the heart for
oxygenated blood.
 Because coronary artery narrowing or
obstruction owing to atherosclerosis cause
myocardial ischemia in the vast majority of
cases, IHD is often termed coronary artery
disease or coronary heart disease.

Pathophysiology of ischemia:
Ischemia occurs due to an imbalance between
i) myocardial O2 supply
ii) myocardial O2 demand
Myocardial O2 supply depends upon the coronary
blood flow and oxygenation of blood. Imbalance
occur by either of two ways—
i) by decreasing the O2 supply without
increasing the O2 demand
ii) disproportionate increase in O2 demand in
relation to the capacity to increase blood flow.
Normally ischemia is precipitated by insufficient
increased in coronary blood flow in response to
an increase in myocardial O2 demand.
Depending on the rate of development and
ultimate severity of the arterial narrowing
and myocardial response, four ischemic
syndromes may result:
i) angina pectoris, of which there are three
variants, the most threatening being unstable
angina.
ii) myocardial infarction, the most important
severe form of IHD, in which there can be
substantial myocardial damage.
 iii) chronic ischemic heart disease with CHF
iv) sudden cardiac death
These syndromes of IHD are the late
manifestation of coronary atherosclerosis.
Because coronary atherosclerosis is a slowly
progressive disease that likely began during
the childhood.
 The dominant influence in the causation of
IHD is diminished coronary perfusion relative
to myocardial demand which is due to—
fixed atherosclerotic narrowing of the
epicardial coronary arteries,
intraluminal thrombosis overlying a ruptured
or fissured atherosclerotic plaque,
platelet aggression and
vasospasm.
Angina Pectoris
 Angina pectoris is a symptomatic manifestation
of IHD characterized by paroxysmal attacks of
substernal chest discomfort (i.e. constricting,
squzeeing, chocking or knife like) caused by
transient (15 seconds-15 minutes) myocardial
ischemia that is insufficient to induce cellular
necrosis
(myocardial infarction). There are three patterns
of angina pectoris:
i) Stable angina
ii) Variant angina
iii) Unstable angina
i) Stable angina—It is the most common form.
The pathogenesis of typical angina pectoris
appears to be the reduction of coronary
perfusion to a critical level by chronic stenosing
coronary atherosclerosis. This render the heart
vulnerable to further ischemia whenever there
is increased demand.
Normally increased demand is produced by
physical activity, emotional excitement or any
other causes of increased cardiac workload.
Typical angina pectoris is generally relieved by
rest(thereby decreasing demand) or
nitroglycerine, a strong vasodilator(thereby
increasing supply).
In particular instances, vasospasm may
contribute to the imbalance between supply
and demand.
 ii) variant angina—It refers to a pattern of
episodic angina that occurs at rest and due to
coronary artery spasm.
Variant angina generally responds promptly to
vasodilators, such as
nitroglycerin and
calcium channel blockers.
iii) Unstable angina—It refers to a pattern of
pain that occurs with progressively increasing
frequency. It is precipitated often at rest and
tends to be prolonged duration.
The ischemia, that occurs in unstable angina
referred to as pre-infarction angina or acute
coronary insufficiency.
In most patients, unstable angina is induced by
fissuring, ulceration, or rupture of an
atherosclerotic plaque with super imposed
partial (mural) thrombosis and possibly
embolization or vasospasm.
Myocardial infarction
Myocardial infarction is almost always due to
the formation of occlusive thrombus at the site
of rupture of an atheromatous plaque in a
coronary artery.
Acute myocardial infarction, also known as
“heart failure” is the most important and
severe form of ischemic heart disease(IHD)
and alone is the leading cause of death in
Bangladesh.
 Pathogenesis:
 Coronary arterial occlusion– The possible
causes of acute transmural myocardial infarct
are-
i) severe coronary atherosclerosis
ii) an acute atheromatous plaque changes
(fissuring, ulceration)
iii) superimposed thrombosis
iv) platelet activation and vasospasm
In addition, increased myocardial demand
(tachycardia) or a drop in BP, can worsen the
situation.
 Myocardial response—Occlusion of a major
coronary artery results in ischemia throughout
the anatomical region (called area at risk)
supplied by that artery, most pronounced in the
subendocardium.
Acutely ischemic myocardium undergoes
progressive biochemical, functional and
morphological changes.
The main biochemical change is the onset of
anaerobic glycolysis within seconds, leading
to accumulation of lactic acid.
Myocardial function i.e. contractility is
decreased within 60 seconds of onset. These
early changes are reversible, and cell death is
not immediate.
Although function becomes strikingly
abnormal within 1 minute after onset of
ischemia, myocardial necrosis occurs only
after 20 -40 minutes of severe ischemia.
Classic acute myocardial infarction with
extensively necrosis occurs when the
perfusion of the myocardium is reduced
severely below its needs for an extended
interval (hours) causing prolonged ischemia
and resulting in cell death by necrosis.
In contrast, if restoration of myocardial blood
flow occurs within 20 minutes, loss of cell
viability does not result.
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