Transcript 8&9-CARDIAC_OUTPUT.ppt

 By
the end of this lecture the students are
expected to:
 Understand the concept of preload and
afterload.
 Determine factors affecting the end-diastolic
volume.
 Explains how cardiac contractility affects SV,
 Ability
of the heart to change its force of
contraction and therefore stroke volume
in response to changes in venous return .
 Also
defined as the ability of the heart to
pump all blood coming to it without
allowing systemic stasis, within limits.
Mechanism of Starling Law:
An increase in preload lead to an increase
in the sarcomere length and increases
troponin C calcium sensitivity, which
increases the rate of cross-bridge
attachment and detachment, and the
amount of tension developed by the
muscle fiber. This increases SV.
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If in a controlled
experimental model right
atrial pressure is varied
(independent variable) and
the cardiac output measured
(dependent variable), you
will find that as PRA is
increased, the cardiac output
(CO) increases.
When the mean PRA is about
0 mmHg (note that PRA
normally fluctuates with
atrial contraction and
respiration), the cardiac
output in an adult human is
about 5 L/min.
Because of the steepness of
the cardiac function curve,
very small changes in PRA
(just a few mmHg) can lead
to large changes in CO .
Increase:
-Stronger atrial contraction.
-Increased total blood volume
-Increased venous tone.
-Increased sk m pump.
-Increased negative intrathoracic pressure.
Decrease:
Standing
Increased intrapericardial pressure.
Decreased ventricular compliance
Afterload
can be defined as the
"load" that the heart must eject
blood against.

The afterload is closely related to
the aortic pressure.

When arterial
pressure is reduced,
the ventricle can
eject blood more
rapidly, which
increases the stroke
volume and thereby
decreases the endsystolic volume.

An increase in afterload, lead
to an increase in end-systolic
volume and a decrease in
stroke volume. An increase in
afterload shifts the FrankStarling curve down and to
the right (from A to B).
Explanation:, an increase in
afterload decreases the
velocity of fiber shortening.
This reduces the rate of
volume ejection so that more
blood is left within the
ventricle at the end of systole
(increase end-systolic
volume)
.A decrease in afterload shifts
the Frank-Starling curve up
and to the left (A to C).
Vascular tone (and therefore blood
pressure)
Aortic stiffness
Myocardial tension (affected by
hypoxia, volume overload)
Preload
Valvular regurgitation
 Aortic
stenosis.
 Arterial hypertension
1. Nervous:
-Sympathetic: HR & SV.
- -Parasympathetic: HR
2. Chemical
-Potassium
-Calcium.
-Thyroxin.
-Catecholamine.
Intrinsic diseases:
i.e. originating within the heart include:
1. dilated cardiomyopathy.
2. hypertrophic cardiomyopathy.
External factors:
These place excessive demands upon the heart:
1.long-term, uncontrolled hypertension,
2.increased stroke volume(volume load; arterialvenous shunts),
3.hormonal disorders such as hyperthyroidism, and
pregnancy.
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Myocardial infarction
Coronary artery disease
Valve disease
Idiopathic cardiomyopathy
Viral or bacterial cardiomyopathy
Myocarditis
Pericarditis
Arrhythmias
Chronic hypertension
Thyroid disease
Septic shock

Acute heart failure develops rapidly and can be
immediately life threatening because the heart
does not have time to undergo compensatory
adaptations.

Acute failure (hours/days) may result from:
1. cardiopulmonary by-pass surgery,
2. acute infection (sepsis),
3. acute myocardial infarction,
4. severe arrhythmias, etc.
 Chronic
heart failure is a long-term condition
(months/years) that is associated with the
heart undergoing adaptive responses (e.g.,
dilation, hypertrophy) to a precipitating
cause. These adaptive responses, however,
can be deleterious
Neurohormonal
mechanisms and
compensatory
mechanisms in
heart failure ,
BMJ 2000;
320:167-170
Reninangiotensin
aldosterone
system in
HF
Effect of
natriuretic
peptide
 Common
respiratory signs :
Tachypnea (increased rate of breathing) and
increased work of breathing (non-specific
signs of respiratory distress).
Rales or crackles, heard initially in the lung
bases, and when severe, throughout the lung
fields suggest the development of pulmonary
edema (fluid in the alveoli).
Cyanosis which suggests severe hypoxemia,
is a late sign of extremely severe pulmonary
edema.
 Additional
signs indicating left ventricular
failure include:
lateral displacement of apex beat
(which occurs if the heart is enlarged)
gallop rhythm (additional heart sounds)
may be heard as a marker of increased blood
flow, or increased intra-cardiac pressure.
 Pitting
peripheral edema,
 ascites,
 Hepatomegaly
 Increased Jugular venous pressure.
The control of congestive heart failure
symptoms, can be divided into three
categories:
(1) reduction of cardiac workload, including
both preload and afterload;
(2) control of excessive retention of salt and
water; and
(3) enhancement of myocardial contractility.
Signs/Symptoms
Left-Sided Heart Failure
Pitting Edema (Legs,
Mild to moderate.
Hands)
Right-Sided Heart Failure
Moderate to severe
Fluid Retention
Pulmonary edema (fluid in
lungs) and pleural effusion (fluid Abdomen (ascites).
around lungs).
Organ Enlargement
Heart.
Neck Veins
Mild to moderate raised jugular Severe jugular venous pressure (JVP).
venous pressure (JVP).
Neck veins visibly distended.
Shortness of Breath
Prominent dyspnea. Paroxysmal
Dyspnea present but not as prominent.
nocturnal dyspnea (PND).
Gastrointestinal
Present but not as prominent.
Liver. Mild jaundice may be present.
Loss of appetite. Bloating. Constipation.
Symptoms are significantly more
prominent than LVF